j0305257 j0305257 Systemic Pathology CARDIOVASCULAR system j0305257 ATHEROSCLEROSIS •disease of large and medium-sizes arteries with lipid deposition into intima •active inflammatory process • •endogennous risk factors, mostly noninfluenceables : –age, MxF (estrogen?), familiar factors (f. hypercholesterolemia), hereditary homocysteinemia ð •exogennous risk factors: –hyperlipidemia (LDL) ←← hypothyreosis, nephrotic sy; –hypertension, diabetes mellitus, life style smoking (nicotine, CO), sedentary life, food + obesity; ↑CRP j0305257 Atherosclerosis - pathogenesis 1.Endothelial injury ð - mechanic (↑BP, turbulence) ð - endotoxins, immune complexes, exogennous toxins (cig. smoke), ↑ cholesterol ð ↑ expression of cell adhesion molecules, ↑ permeability, ↑ thrombogenicity ← 2.Lipoprotein insudation (LDL) – oxidation in intima 3. 3.Inflammation ð - blood monocytes (→foam cells), T-cells, platelets, smooth muscle cells → 4.Repair - proliferation of myointimal cells ð - synthesis of collagen, elastin, proteoglycans → fibrotic plaque, + lipid accumulation - atheromatous plaque ð ð stable plaque under repeated inflammation turns into unstable plaque – fibrous cap + endothelium rupture - thrombus j0305257 3 - patogeneze aterosklerózy.emf 3 - patogeneze aterosklerózy.emf 3 - patogeneze aterosklerózy.emf 3 - patogeneze aterosklerózy.emf 3 - patogeneze aterosklerózy.emf Atherosclerosis - pathogenesis j0305257 atherosclerosis – cell interactions in an atheromatous plaque 4 - buněčné interakce při ateroskleróze.emf j0305257 Atherosclerosis ûfatty streak ûfibrotic plaque ûatheromatous plaque ûcomplicated atheromatous plaque (ulceration, calcification, thrombosis) û j0305257 Atherosclerosis ûSEQUELS: arterial occlusion in situ û chronic (→ hypoxia, atrophy) û acute (→ ischemia, infarction, encephalomalatia) û embolism (thrombus, plaque material) û weakening of arterial wall (aneurysm), risk of rupture û bleeding (from plaque, fissured wall) û calcification (hypertensive factor) û j0305257 Atherosclerosis– fatty streak CV016 _aorta-fatty-streaks-1-330c j0305257 _ath-obliterating-330d Atherosclerosis – fibrous and atheromatous plaques j0305257 _aorta-heavy-athero-330d Atherosclerosis– plaque ulceration, mural thrombosis j0305257 obr01 1 lumen narrowing 2 intimal atheromatous plaque 3 undamaged wall 4 epicardial fat tissue 1 2 3 4 Atherosclerosis– coronary artery j0305257 obr03 1 fibrous plaque in intima 2 vessel lumen 3 media 4 adventitia 2 1 3 4 1 Atherosclerosis – fibrous plaque j0305257 obr02 1 atheromatous plaque in intima 2 vessel lumen 3 media 4 adventitia 5 intimal neovascularization 2 1 3 1 4 5 Atherosclerosis – atheromatous plaque j0305257 obr06 1 vessel lumen 2 media 3 vascularization 4 cholesterol crystals 3 1 4 4 2 Atherosclerosis – atheromatous plaque, intimal neovascularization j0305257 obr07 1 nuclei of foam cells 2 lipids in cytoplasm 1 2 2 Atherosclerosis – foam cells in atheromatous plaque j0305257 C:\Documents and Settings\Patol\Dokumenty\Haškovcová\patologie myokardu\c-1.jpg 1 abdominální aorta 2 trombóza a. mesenterica 3 truncus coeliacus 1 Atherosclerosis – complications thrombosis/thrombembolia 2 3 GI031 4 trombóza koronární a. 4 C:\Documents and Settings\Patol\Dokumenty\Haškovcová\patologie myokardu\d-1.jpg j0305257 aneurysm û localized, blood-filled balloon-like bulge in the wall of a blood vessel. ð the circle of Willis in the brain, thoracic and abdominal aortic aneurysm ð û atherosclerotic aneurysm x syphilitic û û etiology: ð hereditary defects in the structure, atherosclerosis, inflammation, disease process, accidents … ð û false aneurysm û û serpentine aneurysm, arteriovenous aneurysm ð ð ð j0305257 _aorta-abd-aneurysm-330e _aneurysm-circ-willis-331f 3 a. cerebri anterior 4 a. cerebri media 5 a. cerebri posterior 6 a. basilaris 7 aneurysm 1 abdominal aorta 2 aneurysm Atherosclerosis – complications– aneurysm 1 2 3 4 5 6 7 j0305257 ûtear in aortic intima - intramural bleeding through media, false lumen, possible „double-barreled“ aorta û ûtypic in ascending aort, 1–8 cm above aortic valve û ûante– and retrograde spread to the aortic root û ûcommon thrombosis in false lumen û ûrisk of external rupture (è hemoperikardium), progression at the aortic branches (èvariable organ‘s ischemia), heart failure û ûpredisposition – hypertension, Marfan sy, cystic medial necrosis, … Aortic dissection j0305257 typy disekcí Aortic dissection j0305257 disekce aorty Aortic dissection j0305257 VASCULITIS ûVessel wall inflammation û ûClassification according cause: infectious x non-infectious (commonly immune-mediated, ANCA+/ANCA-) û ûAffected organs : all organs with vessels ûType (size) of vessel involved: Large-vessel û Medium-vessel û Small-vessel j0305257 Vasculitis ûANCA+ vasculitis (dangerous, even fatal within a few years, if not recognised) ðWegener granulomatosis ðChurg-Strauss syndrome ðmicroscopic polyangiitis ð ûANCA- vaskulitis: ðpolyarteritis nodosa ðKawasaki disease ðgiant-cell arteritis (Horton, temporal)) ðTakayasu arteritis ðthrombangiitis obliterans (Bürger disease) ðleukocytoclastic (alergic) vasculitis – cca 30% ð j0305257 û ûautoimmune process û ûinfection ðie. streptococcus, … ðdirect cause of infective v., or trigger factor of pathological immune processes Etiology j0305257 ûORL: - repeated respiratory tract inflammation û - exudate rich in plasma cells + eosinophils û ûKidney: - glomerulonephritis û ûLung: - variable presentation of lung diseases + hemoptysis û ûSkin: - ulceration, necrosis, petechiae-purpura û ûGIT: - ischemic ulcerations (sharply demarcated, without HP, minimal inflammation) û ûChronic debilitating disease – clinical signs of tumor!! û Possible clinical signs of systemic vasculitis j0305257 • fever, nausea, myalgia, arthralgia • skin purpura • signs of nephritis • abdominal pain • • • •general malaise (~ severe influenza, long duration, resistant to usual therapy) • sinusoid course (relapse --- remission --- relapse--) • Patient presentation j0305257 D:\SCContent\9781416031215\graphics\fullsize\S9781416031215-011-f022.jpg ANCA PAN Kawasaki Giant-cell a., Takayasu Microskop. polyangiits Wegener Churg-Strauss. sy j0305257 ûincidence ???? ð ≤20/1mil. inhabitants ðage 65+ - 53/1mil. inhabitants ð û ûprognosis: ð untreated ANCA+ vasculitis ≥80% fatal in 2 yrs ð treated ANCA+ vasculitis : ≥80% survives 5 yrs ð renal failure in elders >70 yrs - in 40% due to ANCA+ vasculitis ANCA+ vasculitis j0305257 ûclinically as pneumonitis, persistent X-ray with bilat. nodular infiltrates, chronic sinusitis with mucosal ulcerations nasopharynx (sometimes destructive axial structures), ARI / CHRI (focal necrosis, sickle cell GLN) û ð ð granulomatosis with polyangiitis (Wegener granulomatosis) j0305257 granulomatosis with polyangiitis (Wegener granulomatosis) ûpersistent pneumonitis (95%) – nodular infiltrates û ûchronic sinusitis (90%) – ulcerations, event. Destructive û ûrenal disease (80%) – glomerulonephritis û ûother features: rashes, muscle pains, articular involvement, mono-/polyneuritis û j0305257 D:\SCContent\9781416031215\graphics\fullsize\S9781416031215-011-f026.jpg D:\SCContent\9781416031215\graphics\fullsize\S9781416031215-011-f026.jpg Small vessel vasculitis with giant-cell granulomatous reaction j0305257 ûANCA in approx. 70% (remaining by immunecomplexes or antibodies) û û= necrotizing vasculitis arterioles, capillaries, venules (synonyms: leukocytoclastic v., hypersensitive v., allergic v.) û û: SKIN, kidney, lung, GIT, brain… û ûhighly variable etiopathogenesis (part of systemic connective tissue diseases; alergic response to exogennous antigens – bacteria, viruses, drugs) û ûmicro: ðfibrinoid necrosis of vessel wall with neutrophils and chromatin fragments from neutrophil‘s nuclei - leukocytocllastic) ðall lesions in the same stage of evolution (X polyarteritis nodosa) ANCA+ VASCULITIS: microscopic polyangiitis j0305257 S01871-011-f026b nuclear fragments from neutrophils in a small vessel wall leukocytoclastic vasculitis j0305257 01194+ 1 thrombosed vessel lumen 2 fibrin deposition 3 mixed inflammatory infiltrate 1 2 polyarteritis nodosa 2 1 3 3 3 j0305257 01527+ 1 thrombosed vessel lumen 2 fibrin deposition 3 mixed inflammatory infiltrate polyarteritis nodosa 1 3 2 3 j0305257 2 3 Coronary aneurysms in a child‘ heart coronary artery with lamina elastica interna defects (arrows) and thrombotized aneurysms Kawasaki disease j0305257 S01871-011-f026e 4 Obliterative thrombosis with granuloma with central microabscess (arrow) acral necroses Thrombangiitis obliterans (Bürger disease) j0305257 ûrare û ûarise: ðtransfer of infection from surrounding tissues ðinfected emboli during pyemia û ûexamples: ð aortitis luetica ð bacillary angiomatosis = opportunistic infections (eg AIDS)?? infectious vasculitis j0305257 Infectious vasculitis ûdirect invasion of vascular wall by inf. pathogen û ûprimary angioinvasive microorganism û Fungi: Aspergillus, Mucor - thrombosis→ ischemic necrosis û ûsecondary vasculitis - localized vasculitis in focal infection ðpurulent – meningitis ðpneumonia ðabscess, fasciitis – pyogenic bacteria ð granulomatous •obliterative endarteritis – TBtertiary syphilis, l •Lepra ð lymphocytic vasculitis – rickettsia (spotted fever, Q fever etc.) ð recurrent herpes, CMV ðnecrotizing vasculitis – anthrax ð ð ð ð ð • û j0305257 j0305257 Cardiac pathology j0305257 Morphology ûpericardial sac – cca 30ml clear yellowish fluid û û male = 300 – 350 g, ð - hypertrophy > 400g û û myocardium: û è RV 3 – 4 mm û è LV 12 – 15 mm û û foramen ovale ð - closed x opened è paradoxical embolia è srdce6 j0305257 Systemic hypertension and heart û90–95% essential , risk factor for AS û ûwork overload è LV adaptation to peripheral resistance = cor hypertonicum (concentric LV hypertrophy) è limited compensatory mechanisms è cor hypertonicum decompensatum (dilatation of hypertrophic LV) û ûè heart insufficiency á relative coronary incompetence hypertrofie myokardu LKS j0305257 Heart failure û heart unable to pump blood at a rate sufficient for metabolic demands of the tissues û û systolic dysfunction - ↓ myocardial contractile function (ischemic injury, pressure or volume overload – valvular disease, hypertension, cardiomyopathy û diastolic dysfunction - inability to dilatate sufficiently (massive LV hypertrophy, myofibrosis, amyloidosis) û û cardial – extracardial pathologic changes j0305257 Heart failure û failure of normal pumping action of the heart û failure of forward and backward è to cardiogenic shock û manifestations of the heart and heart out j0305257 Cardial changes û ûdisproportion between heart function and peripheral vascular resistance û û differ according rapidity of development: û – sudden è acute dilatation û û – chronic è adaptation è è è û myocardial hypertrophy ( nutritional demands) +/- ventricular dilatation (enhanced contractility – Frank-Starling mechanism), + activation of neurohumoral systems (norepinephrin, renin-angiotensin sy, atrial natriuretic peptide û j0305257 Extracardial changes ûvenoous congestion – e.g. liver (-> hepar moschatum) û ûinduration – fibroproduction (liver, spleen, kidney) û ûoedema – û ûcyanosis – visible on acral parts j0305257 Chronic venous congestion (nutmeg liver - hepar moschatum) j0305257 Hepatic venous congestion městnání v játrech 20x 1 2 2 1 1 1 Portal spaces 2 Congestive lines (severe congestion with hepatocyte necrosis) --- pseudolobule: confluent remnants of 3 lobules, centrally portal space j0305257 Pulmonary oedema edem plic 100x 1 oedematic fluid 2 widening of septa 3 capillary dilatation 1 1 2 3 j0305257 chron venostáza plíce Chronic pulmonary venous congestion 1 1 1 oedematic fluid è hyperemic septa Æ siderophages j0305257 Ischemic heart disease (IHD) ûgroup of pathophysiologically related syndromes resulting from myocardial ischemia (hypoxia or anoxia, ↓ nutrients, ↓ removal of metabolites) û ûimbalance between the demand and supply by coronary arteries. û û important factor – coronary AS û û forms: ðangina pectoris ðmyocardial infarction (MI) ð chronic IHD with heart failure ð sudden cardiac death j0305257 Pathogenesis of IHD 1)AS of coronary aa. û – commonly at a. branching û – fixed obstruction by plaque (fibrous, atheromatic) û – acute plaque change (rupture, erosion, haemorrhage, thrombosis) û – 75% stenosis – ischemia during á workload – stable angina pectoris û – 90% stenosis –ischemia even at rest – ustable angina - preinfarction û û2) non-atherosclerotic û – coronary emboli – endocarditis, atrial fibrillation, mural thr., paradoxical e. û – coronary vasospasm û – aortic dissection û – coronary vasculitis û – congenital coronary aa. defects û –hematologic disorders, amyloidosis, shock, etc. û û û j0305257 ischemic heart disease (IHS) ûMorphology of myocardial ischemia: ðsteatosis myokardu ð myomalatia (= partial necrosis – cardiomyocytes only) ð dispersive /confluent myofibrosis ð myocardial infarction: transmural/subendocardial (complete coagulative necrosis incl. interstitium) û disp..JPG 1 cardiomyocytes 2 myofibrosis 3 vessels j0305257 Confluent myofibrosis and myocard lipomatosis P0012.jpg P0011.jpg 1 bearings confluent myofibrosis 2 hypertrofic cardiomyocytes 3 adipose tissue 2 2 1 1 3 j0305257 Angina pectoris (AP) û transient myocardial ischemia è chest pain !!! - û1. stable (typical) û – due to increased workload, duration ≤ 15 min, relieved by rest or nitroglycerin û – no myocardial necrosis û –subendocardial LV myocardium û û2. unstable û – increasing frequency / duration of pain attack, even at rest û – plaque disruption + mural thrombosis, possible vasospasm û – preinfarction angina û û3. variant (Prinzmetal) angina û – mostly unrelated to physical activity, coronary vasospasm - vasodilatative therapy û û û j0305257 Myocardial infarction û ischaemic coagulative necrosis û û causes: ð usually coronary thrombosis ð complicated atheromatic plaque ð event. embolism ð spasm ð inflammation ð rarely systemic causes. û ûgross ð evolution; first signs (red, softer) after 12 hrs ð 2-3 days established infarction (yellowish, haemorrhagic rim) ð weeks – formation of firm white fibrotic scar û û j0305257 Myocardial infarction û micro: ð necrotic cells more red ð loss of nuclei and striation ð neutrofils ð later macrophages in stroma ð reparation by granulation tissue -> scar û j0305257 Myocardial infarction ûmicro: û12-24 hr: edema, hypereosinophilia of necrotic cells, pyknosis û û1-3 days: neutrophils, loss of nuclei û û3-7 days: macrophages at the border, desintegration of myofibers û û1-2 weeks: repair by granulation tissue û û cca 2 months: scar û j0305257 _myoc-fresh-ihf-322a 1 subendocardial coagulative necrosis 2 hyperemic rim 3 normal myocardium 4 epicardium 2 Myocardial infarction 1 1 2 4 3 j0305257 obr10 1 myomalatia 2 normal cardiomyocytes 3 myofibrosis 1 1 2 3 Myomalatia j0305257 1 3 2 5 4 1 coagulative necrosis 2 myomalatia 3 hyperemic rim 4 neutrophils 5 regressive changes Microscopic changes in developed MI j0305257 Myocardial infarction ûtransmural (QIM, STEMI) - + ST elevation on ECG û – ≥ ¾ of wall thickness, breadth >25 mm û – complete coronary artery obstruction û emergency angioplasty/stenting û û non-transmural (subendocardial, Non-STEMI) û – internal ¼ až ½ of LV wall û – collateral bllod flow, incomplete obstruction, shorter ischemia j0305257 MI complications 1.sudden death (arrythmia) 2.cardiogenic shock (contractile dysfunction) 3.pericarditis epistenocardiaca ð -> sero-fibrinous inflammation 4.mural thrombosis ð -> embolism into systemic circulation (-> brain, kidney, intestine, spleen infarction) 5.ventricular aneurysm ð -> acute – risk of rupture, trhrombosis; chronic – LV insufficiency 6.cardiac rupture ð -> free wall, septum, : tamponade / acute heart failure 7.papillary muscle rupture ð -> valvular incompetence → acute heart failure j0305257 _heart-infarct+thrombus MI – mural thrombosis j0305257 _heart-ruptured-wall-inf Mi – rupture j0305257 _cardiac-tamponade-2-66e _cardiac-tamponade-1-66e 1 lung 2 pericardial sac 3 blood coagulum 4 thoracic wall 3 1 2 1 1 4 4 MI – rupture, tamponade j0305257 CV143 1 aneurysm w. thrombosis 2 RV 3 LV 4 mitral valve 4 1 2 3 MI – LV aneurysm j0305257 Chronic ischemic heart disease (IHD) ûangina pectoris or MI in anamnesis û ûprogressive heart failure due to ischemic myocardial damage è LV failure è congestive RV failure û ûheart hypertrophy + dilatattion, myofibrosis and/or post-MI scars û ûmultiple coronary arteries with significant AS stenosis û ûimminent risk of MI, sudden cardiac death due to arrythmia, heart failure j0305257 Sudden cardiac death û= unexpected death from cardiac causes, without preexisting symptoms or within 1 hr of the onset of symptoms û ûmost commonly due to lethal arrythmia (ventricular fibrillation, asystole) û ûsudden collapse without signs of acute MI û ûother causes: ðdissecting/ruptured aortic aneurysm ðpulmonaty thrombembolism ðmassive intracerebral haemorrhage ðheritable conditions incl. anatomic, electriical – channelopathies ð ð û û j0305257 Endocardial / valvular diseases û ûendocarditis ðinfectious or immune-mediated endocardial inflammation ð ûdegenerative diseases ðcalcific aortic (rarely mitral) stenosis, mitral valve prolapse, annular and marginal sclerosis ð ûendocrine diseases ðcarcinoid syndrome û ûnonbacterial thrombotic endocarditis (in debilitated patients) û j0305257 Infective endocarditis û ûcommonly by highly virulent microorganisms ðStrep. pyogenenes, Strep. pneumoniae, Staph. aureus, … ev. fungi ð ûsubacute IE – less virulent microorganisms ðviridans streptococci ûpredisposition: ðdeformed valve, bioprosthesis, postcatethrization, i.v. drug addicts û û ûbacteremia - endocardial damage by bacteria - trombosis = infective vegetation û ð j0305257 Infective endocarditis ûgross: friable red-brown mass 0,5-2 cm on leaflets or chordae tendinae, valvular damage incl. ulceration û û ûmicro: ð fibrin + bacterial colonies + neutrophils (+ granulation tissue) ð Inflammation/ necrosis of the valve tissue ð ð ûcomplications: ð acute: valvular damage, myocarditis + abscess, pyemia,thrombembolism ð chronic valvular disease û j0305257 _heart-endocarditis-bacterial-valve-destruction 1 vegetation 2 endocardium 3 papillary muscle 4 myocardium Infective endocarditis– valve destruction 1 2 3 4 j0305257 Infective endocarditis 9 - IE.emf Mi vegetations Ao valve destruction purulent inflammation IE repair (Mi fenestration without vegetations) j0305257 obr20 1 bacterial colonies 2 trombus 3 red + white blood cells 1 3 Infective endocarditis - vegetations 1 1 2 j0305257 Infective endocarditis - vegetations endocarditis 100x.jpg 1 1 2 2 3 3 1 bacterial colonies 2 trombus 3 inflammatory infiltrate j0305257 obr21 1 bacterial colonies 2 valve neutrophilic infiltrated granulocytes Infective endocarditis - vegetations 1 2 j0305257 Non-bacterial thrombotic endocarditis ûsterile vegetations due to hypercoagulative state Þ concurrent venous thrombosis and lung embolization û ûin generalized malignancies, chronic nephropathy with uremia, COPD etc. û ûmostly on mitral valve (normal) û ûmicro: verrucous vegetations (single or multiple), 1-5 mm, bland thrombi û û ûpossible source of emboli j0305257 _endocarditis-nonbacterial-thrombotic 1 mi valve 2 endocardium 3 papillary muscle 4 trombi 5 myocardium 2 1 3 4 4 4 5 Non-bacterial thrombotic endocarditis j0305257 Rheumatic fever, rheumatic heart disease ûacutenon-purulent, imunne-mediated systemic poststreptococcall inflammation (cross-reactive antibodies) û ûacute stage: PANCARDITIS ðfibrinous pericarditis + myocarditis with Aschoff bodies (foci of fibrinoid necrosis + inflammatory reaction + verrucous endocarditis (small depositions of fibrin along the closure lines of Ao a Mi valves) ð ðacute endocarditis commonly recurrent ð ûchronic stage: ð diffuse fiubrous thickening + distortion, commisural fusion → dystrophic calcifikacation - stenosis + incompetence) ð û j0305257 7 - revmatické postižení srdce.emf rheumatic heart disease Verrucous endocarditis Aschoff body 7 - revmatické postižení srdce.emf Commisural fusion j0305257 Carcinoid syndrome endocardial fibrous plaquelike thockenings – RA, RV j0305257 Myocarditis ûmyokardial inflammatory damage without ischemia û ûgross: ð cardiac dilatation, flabby, mottled myocardium û û micro: ðinflammatory infiltrate (acccording etiology) + cardiomyocyte regressive changes incl. necrosis û û etiology: ð viruses, ricketsia, chlamydia, bacteria (diphtheria, sepsis), fungi, protozoa (toxoplasmosis), helminths (trichinosis) ð immune-mediated (drug hypersesitivity, postviral, rheumatic fever, rejection) ðionising radiation ðunknown (giant-cell myocarditis j0305257 Viral myocarditis û Coxsackie, parvovirus B19, influenza, EBV, CMV, HIV û ûinflammatory infiltrate: T-cells mostly û û after acute attack commonly autoimune-mediated cardiomyocytes destruction û and fibrosis → dilated cardiomyopathy û û j0305257 Viral myocarditis û myokarditida 100x.jpg myokarditida 40x.jpg 1 cardiomyocytes 2 lymphocytic infiltrate in interstitium 2 2 2 1 1 j0305257 myokarditida 400x.jpg Viral myocarditis 1 cardiomyocytes 2 lymphocytic infiltrate in interstitium 1 1 2 2 j0305257 Septic myocarditis CV053 1 cardiomyocytes 2 bacterial colony 3 neutrophils 1 2 3 1 1 3 3 j0305257 Cardiomyopathies û= heart disease due to myocardial abnormality, with heart dysfunction ûdiagnosis after exclusion of IHD, valvular disease, congenital d. or hypertension û ûheterogenous group of disorders: ð dilated (DCM) •– dilatation + hypertrophy,¯ LV contraction, possible mural thrombosis; 20–50% genetic (AD); alkoholic, peripartum, myocarditis... ð hypertrophic (HCM) •– massive LV hypertrophy, 100% genetic, diastolic dysfunction, histologic „disarray“ ð restrictive cardiomyopathy • – diastolic dysfunction, ¯ of compliance - ¯ filling, myocardial stiffness ð specific CM •– Duchenne muscle dystrophy, toxic (drugs), endocrine d., metabolic d. (hemochromatosis, amyloidosis, glykogenosis,…) û û j0305257 Myocardial amyloidosis ûlocal x systemic (mostly AL amyloidosis) û ûsenile amyloidosis ðatrial + ventricles; amyloid protein = prealbumin (transthyretin) û ûisolated atrial amyloidosis ð amyloid protein = atrial natriuretic peptide û ûgross: consistency normal - firm (rubbery) û ûmicro: variable amyloid deposits v interstitium and vessels, Congo red + polarization û û j0305257 obr13 Senile cardiac amyloidosis 1 normal cardiomyocytes 2 deposits amyloid 1 1 2 2 2 2 j0305257 1) û 1) Pericardial effusion û - transudate in congestive heart failura or hypoproteinemia, slow (up to 500ml – pericardial dilatation) û û û 2) haemopericardium û – wall rupturein MI or aortic root dissection è fatal cardiac tamponade û û û diastolic filling restriction • Pericardial pathology j0305257 Pericardial pathology û 3) Inflammatory exudate in pericarditis: û ða) non-infectious û – pericarditis epistenocardiaca, uremic, post-operative, SLE, Dressler sy (post-MI autoimmune) û û b) infectious ð – haematogenous, direct spread, lymphogennous; variable agents ð ðc) idiopatická û û Pozn. hojení – serózní a část. i fibrinózní exsudátè vstřebávání x zbývající fibrin se organizuje è perikardiální adheze /konstriktivní perikarditida (pericarditis petrosa) è omezuje plnění komor û û û û j0305257 fibrinous pericarditis fibrińozní perikarditis 20x.jpg fibrińozní perikarditis 100x.jpg 1 1 1 1 fibrinous exudate j0305257 j0305257 Cardiovascular tumors j0305257 Capilary hemangioma 1 1 - capillaries 2 - endothelium 3 – red blood cells 2 3 j0305257 Cavernous hemangioma ûgross: ðred -blue focus (nodular) ðpossible large size (-15 cm) ð liver, spleen, skin; commonly multiple ûmicro: ðlarge blood-filled vascular spaces divided by fibrous septa j0305257 Cavernous hemangioma kavernózní ham 1 septa 2 vascular spaces 2 2 1 j0305257 Kaposi sarcoma - 11 - Kaposi makro j0305257 Kaposi sarcoma ûclassic form ð chronic ð in mediterranean or jewish origin ð usually (90%) confined to skin ð ûendemic ð south-african children ð lymphadenopatic ð aggressive ð ûimmunosuppression (transplant) associated ð – internal organs in 50% û ûAIDS associated j0305257 Kaposi sarcoma ûHHV-8 ûhyperproliferation of endothelial cells ûprevention of apoptosis û ûgross: ð red to purple patches ð raised plaques ð nodules ð ûmicro: ðirregular blood spaces ð plump atypical endothelial cells ðperivascular aggregates of spindle cells j0305257 Kaposi sarcoma 12 - Kaposi, HE fusicellular proliferation, hyaline globules, hemosiderin j0305257 ûprimary tumors rare, mostly benign myxomas û û ûmalignant mesenchymal (sarcomas) ðleiomyo - , rhabdomyo - , hemangio - , fibrosarcoma û û ûsecondary tumors ð20-30 x more common than primary ðmetastases + infiltrates : lung, breast carcinomas, malignant melanoma, malignant lymphomas and leukemias ð direct spread (lung ca, mesothelioma, renal ca) ðpericarditis carcinomatosa – hemorrhagic effusion û Heart tumors j0305257 14 - myxom srdce LV myxoma j0305257 Myxoma (100x) myxom 100x.jpg 1 stellate cells 2 myxoid matrix 3 hemosiderin deposits Textové pole: 1 1 1 2 2 3 j0305257 Myxoma (400x) myxom 200x.jpg 1 stellate cells 2 myxoid matrix 1 1 2 2 j0305257 Angiosarcoma 13 - angiosarkom CD31 RV angiosarcoma j0305257 Angiosarcoma 1- mitoses 1 1