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04/26/22 1 BLOOD AND LYMPHATIC VESSEL Dr.H.Joko S.Lukito, SpPA Dept. Pathology Anatomy FK USU

CVS2 - K35 - K53 - Blood & Lymphatic Vessel PA

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Blood and Lymphatic Vessel

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  • BLOOD AND LYMPHATIC VESSELDr.H.Joko S.Lukito, SpPADept. Pathology AnatomyFK USU

  • ARTERYCONGENITAL ABNORMALITIES Especially aorta & large arteries Generally are assosiated with congenital heart disease

    Ascending aorta hypoplasiaAortic arch anomalies- Aorta coarctation- Patent Ductus Arteriosus- Right Subclavian artery posterior- Aortic arch on the right- Double aortic arch

  • Degenerative DiseaseAtheromaArteriosclerosis

    Atheroma Normal ArteriosclerosisDeposition of yellow lipid Tunica intima Generalisedmaterial in plaque under Tunica elastica degenerationthe intima Tunica media media Tunica adventitia

  • Degenerative Disease of the VesselArteries IschaemiaVeins/lymphatic congestive edema

    Symptoms :- Functional disorders- Pain, due to :- Infarction- Trophic disorder- Skin ulceration

  • Arteriosclerotic disease = arterial hardening

    Atherosclerotic lipid deposition under the intimaMonckeberg sclerosis calcification on tunica mediaArteriosclerosis in small arteries

  • PathogenesisThe developmental of focal areas of chronic endothelial injuryIncreased insudation of lipoproteins into the vessel wall, mainly LDL or modified LDL with its high cholesterol content A series of cellular interactions in the foci of injury involving ECs, monocytes/ macrophage, T lymphocytes, and SMCs of intimal or medial origin

  • Proliferation of smooth muscle cells in the intima with formation of extracellular matrix by the SMCs.

    Chronic endothelial injury ( hyperlipidemia, hypertension, smoking, etc) endothelial dysfunction ( increased permeability, leucocytes adhesion) monocytes adhesion and emigration smooth muscle emigration from media to intima, macrophage activation

  • macrophage and smooth muscle cells - engulf lipid, macroscopically as fatty streaks smooth muscle -prolliferation, collagen and other ECM deposition , extra selluler lipid ( so called fibrous cap ) fibrofatty atheroma fibrous plaques

  • NORMAL OF BLOOD VESSEL

  • ATHEROSCLEROTIC IN BLOOD VESSEL

  • Atheroma - Coronary heart disease - cerebrovascular accident - extremities gangrene

    Major risk factor : Hypertension Hypertension Cigarette smoking Diabetes

  • Minor risk factor : Insufficient reguler physical activity Stress Obesity The use of oral contraceptive Hyperuricemia High carbohydrate intake Hyperhomocysteinemia

  • Clinical manifestation caused by ischaemic pain growth disorder skin ulceration

    Arteriosclerosis complication :Blood vessel occlutionSkin ulcerationThrombosisEmbolism

  • 2. Monckeberg sclerosis medial calsificationon tunica media + internal lamina elastica of arteries grouping Ca sedimentationAging process

    elastic tissue of intima arranged like onion skin appearance Subintimal hyaline sedimentation.3. Arteriosclerosis arteriole sclerosis

  • INFLAMMATION OF ARTERIESAcute Infectious ArteritisEtio : - Perivascular inflammation : acute meningitis, cellulitis, pneumonia - Intravascular : septicaemia, septic embolism.

    2. Periarteritis nodosa = polyarteritis = panarteritis

  • Clinical manifestations :- intermitten fever- malaise, lethargy- loss of body weight- peripheral neuritis- myalgia, progressive arthralgia

    Male >> femaleAt all ageBody organs which are involved : kidney, brain, heart, skin, lung

  • Macroscopic finding : protruding mass 2-4 mm along the arteries specially in a. mesenteric, GIT, pancreas, kidney, striated muscle.Microscopic :Oedema with fibrinous exudate Fibrinous necrotic mediaDamage of internal elastic laminaWBC infiltration in arterial wallFibroblast proliferation

  • Periartheritis Nodosa :The ConsequencesLuminal obliterationThrombosisAneurysmInfarct

  • Spesific arteritisSyphylitic arteritisTuberculosis arteritis with tubercle central necrosis surrounded by lymphocyte cells, epitheloid cells, plasma cells, and Langhans datia cells.Rheumatoid arteritis fibrinoid necrosisDatia Cells arteritis = Giant cell arteritis temporalis arteritis

  • Datia Cells ArteritisClinical manifestation :Fever Occurs especially in elders (>50yrs old) Temporal, occipital and skull arteries segmental inflamationLeucocytosis, BSR increasedCauses blindness in chronic inflamation (months)

  • Datia Cells ArteritisEtiology: unknown

    Microscopic : - Inflamation reaction on media and internal elastic lamina of the vessels- Datia cells (+)- Fibrosis of the intima- Thickening of the adventitia

  • 5. Takayasu disease = pulseless disease = Aortic arch syndromeClinical appearance :- pulseless disease- chronic and progressive- occurs especially in young women- visual disturbances- upper extremities parasthesia- lethargy (general weakness)-syncope

  • Takayasu diseaseMicroscopic :- pan-arteritis- thickening of the intima- coagulative necrosis- plasma cells , lymphocyte and datia cells inflitration- fibrosis- perivascular infiltration

  • Peripheral Arterial DiseaseI. Arteriosclerosis = arteriosclerosis obliterans Clinical findings : - ischemic atrophy- cold and painful- cyanotic- extremities soft tissue gangrene from distal toes to the proximal legs- muscle spasm- claudicatio intermitten- pale lower extremities when elevated

  • Pathology

    - occurs in midlife and elders- luminal narrowing- thrombotic obstruction- uneven thickening of the artery, hardening but fragile- Iliac artery, femoral artery, poplitea artery, tibial artery.- complicated in diabetes mellitus, hipertension and artherosclerotic patients.

  • 2. Raynaud diseaseA vasospastic syndrome caused by freezing , restricted on fingers only.

    Young women

    Etiology : blood vessels spasm

  • Clinical findings- distal fingers paleness- tingling/ numbness and hot - cyanotic and alternate reddening- can progress to ichaemic necrotic fingers

  • II. Scleroderma = Progressive Systemic SclerosisA systemic diseaseEspecially effected the skinFibrosis in the internal organ30-50 years old Female >>

  • III. Buerger disease = Thromboangitis obliterans (Wini Warter ) young male , heavy smokers persistent painful legs, cause by distal arterial obstruction and occlusion persistent ischemia of 1 or more toes superficial thrombophlebitis

  • Macroscopic : Wire like blood vessels (hardening)

    Blood vessels occluded by yellow/ grayish mass due to thrombosis

    Perivascular fibrosis

  • Microscopic :- thrombus filled lumen- intact elastic lamina- lymphocyte infiltration of media & adventitia- widening of vasa vasorum- fibrosis of adventitia- granulomatous focal with datia cell or supurative milier focal

  • Aneurysmlocal abnormal dilatation of the artery due to wall defect.

    Etiology : - artheriosclerosis- syphilis , bacterial or fungal infection- congenital- trauma

  • Clinical form of aneurysm :- sacculer- fusiform- cylindric- dissecans- circoid / racemosus

  • Favorite localization :- aortic arch- abdominal aorta- popliteal artery- femoral artery- carotid artery or subclavia artery

  • Complication :- rupture- hemorrhage- compression to other organ - erosion

  • VeinsInflamation Acute phlebitis :

    Purulent phlebitis : Abcess, meningitis, pneumoniaNon Purulent phlebitis : dermatitis, rheumatoid fever, drug allergy, rheumatoid arthritis

  • Microscopic : - Inflamation cell infiltration - oedema - hyperemia - blood vessel wall destruction

  • Vein Obstruction AbnormalitiesPhlebothrombosisVein thrombosis without regional blood vessel destruction.ThrombophlebitisThrombosis cause vessel wall destruction.

  • V. Cava Superior Obstructiondue to : bronchogenic Carcinoma mediastinal lymphoma Aortic aneurysmcausing : cyanotic and congestion of cephalic v, neck and upper extremities v.Vena Cava Inferior Obstructiondue to : liver tumor and renal cell Ca. aneurysm ascites and inflamation

  • 5. Portal vein Obstruction due to : thrombosis intrahepatic diseases splenectomy polycytemia vera

    Varicose vein = Varix abnormal vein dilation which restricted due to intraluminal pressure increamentand loss of surrounding tissue support.

  • Etio : hereditary weakness vein obstruction intraabdominal pressure >> elderly people standing too much, hard work vein inflammation chronic constipation

  • Portal hypertension hemorrhoid oesophageal varices

    Frequently on superficial vein of lower extremities.

  • HEART DISEASES

    1. Coronary heart disease 80%2. Hipertensive heart disease 9%3. Rheumatic heart disease 2-3%4. Congenital heart disease 2%5. Bacterial endocarditis 1-2%6. Sifilitik heart disease 1%7. Cor pulmonale 1%8. Another heart disease 5%

  • Coronary heart disease

    All of myocardium disorders due to a. coronary insuffisience - arterisclerosis 99%- rheumatica- sifilis- arteritis- polyarteritis

  • Variant of coronary heart disease :Arteriosclerotic heart disease Angina pectorisMyocardial infarction

    Influenced by :Flow of a. coronarySensitivity myocardium toward ischaemiaO2 concentration of blood

  • Condition associated to CHD : Hypertension Obesity Hypercholesterolemia Smoking DM

  • Ad.1. Coronary insufficiency due to : a. Aortitis luetica b. Granulation tissue of proximal a. coronary c. A. coronaria aneurysm d. Buerger disease e. Polyarteritis nodosa/ Rheumatica

  • Ad.2. Activity of myocardial influenced by : a. Hyperthyroid b. Pregnancy c. Hypermetabolic, febris d. Exercise

    Ad.3. O2 concentration : a. Severe anemia b. Erytrocyte disorders, polycythemia c. Cyanosis

  • Predisposition factors :Lipoprotein serum , soft drink, obesity, alkoholIncreased blood pressureIncreased blood glucoseStressLack of exercise SmokingUric acid serum

  • Arterioscerotic Heart diseaseArterioscerotic of a. coronary & myocardial fibrosis diffuse & sometimes with valve fibrosis.

    Morphologic : Arterioscerotic muscle ischaemia myocardial fibrosis as diffuse grey plaque ...

  • contd :myocardium fiber atrophy and contain lipochrom = Brown atrophy so that cor becomes : smallnormalswelling (in DC)

    Valve abnormalities : mitral valve fibrosischorda tendinea fibrosiscalcification

  • Clinical Manifestation :

    asymptomaticold age with angina pectorismitral / aortic murmurdamage myocardium on ECGheart congestivearrhythmia and myocardium infarction

  • ANGINA PECTORIS

    Is the clinical symptom markedly temporary paroxysmal pain attack in substernal or precordial and commonly arise after exercise and disappear in rest.Myocardium damage not appearnormal at ECG

  • Basic : Myocardium hypoxia due to :coronary arteriosclerosismyocardium lueticapolyarthritis nodosaaortic valve insufficienceAnemia

    Hypoxia caused by : small arteri occlutionarteri spasmWhile exercising paroxysmal myocardium hypoxia

  • MYOCARDIUM INFARCT ( MCI )Coronary insufficiency due to :

    coronary arteriosclerotic 99 %thrombosis and embolismdisease of vesselsnarrowing ostium due to syphilis arteriosclerose and hypotension.

  • MCIPredilection :right a. coronary 40 %left anterior a. coronary 40 %left ventricle

    Morphology :Restricted on central myocardiumMyocardium : epicardium + endocardium becomes thick ( 3 4 cm).Zahn Infarction, subendocardial small lesion

  • Myocardium Infarct Progressivity :< 12 hours: vague or pale 18 - 24 hours: clearly anemic, brown-gray, stable muscle consistency. 2 4 days : well defined necrotic tissue border surround by hyperaemic area, soft, yellow in colour, due to fatty changes4 10 days : progressive fatty degeneration, central nekrosis, soft ,haemorrhage (grayish yellow), well -defined border6 weeks : fibrosis

  • Microscopic :blood vessel ischaemic coagulative necrosis in myocardium cellinterstitial edemahaemorrhage / haemosiderin pigmentneutrophyl exudationfibrosis

  • Complication :Pericarditis fibrinosa / haemorrhagicaMural Thrombosis embolismRupture infarction heart tamponadefibrosis and aneurysm

  • Lab : Nekrosis coagulativa enzyme dehidrogenase glutamic oxaloacetic transaminase

    12 24 hoursSGOT Leukositosis BSR LDH C Reactive Protein

  • Clinical Manifestation :Sudden and deep pain on substernal and precordial.Pain referred to left back , arm to fingers and chin.Pressed feeling, sweating , nausea, vomitLoss of energyBlood vessel to shockDyspnoe

  • CyanoticHeart arrhythmiaECG : - Q abnormal- ST elevation - T invertedDeath rate : male >> 2 x female

    Incidence : Male : 33- 35 years Female : after menopause

  • HYPERTENSIVE HEART DISEASEMarkedly by left ventricle hypertrophy due to continous systemic hypertensive.

    Incidence : Female >> 2x male Middle age and old age Genetically inherited

    Etiology :Hypertensive occur if arterial peripheral resistence

  • Peripheral resistence increased due to : vasoconstriction blood vessel arteriole, small arteries.diffuse organic blood vessel disease

    Hypertensive hyperthrophy myocardium coronary arteriosclerotic Peripheral resistence heart will compensate cardiac output to normal hyperthrophy myocardium swelling left ventrikel dilatation

  • Muscle hyperthrophy caused by :activity >> anoxia myocard weaknesshypertension coronary arteriosclerosis myocardium anoxia.hypertension damage renal blood vessel Renin NaCl + H2O retention

  • Morfology :left ventricle wall >> ( 2,5 cm )heart weight >>without other heart disordersmicroscopic : normal cardiac musclethickened arterial wall

  • Clinical manifestation :Compensatory stadium : asymptomHypertensive symptom : headache, palpitation, retinopathyLeft decompensatio cordis : dyspnoe, cough, hemoptysisCoronary arteriosclerose symptom

  • RHEUMATIC HEART DISEASERheumatic fever is the non supurative systemic inflammation disease. Associated with streptococcus beta haemolitycus group A infection and the immunology reaction with febrile attack and prolonged remission.

  • Rheumatic fever is the collagen disease, can occur in : joint, heart, skin, serous,lung blood vessel

  • Incidence : age 5 15 years 90 %Low economicsOvercrowded area, poor sanitation Low nutrition

  • Rheumatic Inflammation Changes:

    mucoid degenerationfibrinoid necrosishyaline collagen degeneration

  • Etiology:Rheumatic fever arise after 1 - 4 weeks , after infected by streptococcus ( Pharyngitis, Tonsilitis, Scarlatina ) Antigen- antibody reaction causing focal allergic necrosis.markedly by ASTO level

  • Morphology :Specific disorders and pathognomonic : Aschoff body focus fibrinoid degeneration surrounded by inflammation cell infiltration.Focus can be found in : - heart, - Synovial joint, - fascia tendon.Vegetation nodule can be found in skin, subcutis 1 -4 cmSubcutaneous nodule

  • mitral, aortic valve : fibrotic vegetation, calcificationtricuspidale valve : stenosisChorda tendinea : shorten and thicken

  • Clinical Manifestation :

    Major Criteria of Jones:1. Polyarthritis migrans 85 %2. Carditis 65 %3. Chorea sydenham4. Subcutaneous nodule5. Erythema marginatum

  • Minor Criteria of JonesLeucocytosisBSR ASTO FeverArthralgiaProlonged PR intervalErythema

  • Cause of death :Decompensatio cordisBrain/ renal thromboembolismBacterial EndocarditisMitral stenosis

  • COR PULMONALEThe right ventricle hypertrophy, due to pulmonale disorders :Etiology :Acute massive pulmonary embolism, so that dilatation right ventricleChronic 1. Pulmonary disease 2. Chronic pulmonary disease 3. Thorax abnormalities

  • Ad.1. - Diffuse big/small arteries trombosis - Embolism - Diffuse vasculitis - Fibrosis : - sarcoidosis - radiation - asbestosis - berryliosis

  • Ad.2. - Emphysema - Chronic bronchitis - Pulmonary fibrosis due to TBC - Sarcoidosis - Severe pneumonia - Pulmonary resection

  • Ad.3. Thickness pleura bilateral - Neuro abnormalities :PoliomyelitisMyasthenia gravisMuscle distrophyKyphoscoliosis

    Clinical Manifestation :- dyspnoe- dilatation of vein- oedema- ascites- hydrothorax- hepatosplenomegaly

  • CONGENITAL HEART DISEASEEtiology :UnknownGeneticsInfection virus rubella, lues, toxoplasmaDrug teratogenic thalidomide, cortison, busulfan

  • Rogers disease= ventricle septal sefectManifest in IV-VII weeksMacros : - defect, mmcm - right ventricle >> - thickening endocardium parallel of defect Clinically : - hard systole murmur = machinary murmur - pulmonary hypertension - tardive cyanosis

  • Death because of : - right disease - endocarditis

  • 2. Atrium Septal DefectOver IV weeksDefect of foramen ovaleClinically : - cyanotic right sided overload - hypertrophy right ventricle - pulmonary hypertension - systolic murmur

  • 3. Lutembachers disease ASD + Stenosis mitral, right & left ventricle dilatation, hypertrophy right ventricle

    4. Tetralogi FallotDefect septum interventricleDextroposed overriding aortaStenosis pulmonal valveRight ventricle hypertrophy

  • Clinical manifestation : cyanosis from newborn clubbing of the finger growing disorder

    Bad Prognose, cause of death :Right DCEndocarditis bacterialisBrain abcessRespiratory Tr. Infection

  • 5. Eisenmenger ComplexVariant of Tetralogi Fallot without Stenosis Pulmonalis

    6. Patent Ductus Arteriosus From ductus Botalli connected with a. pulmonale & aorta - Ductus Botalli be closed at 1-2 yrs after borned- The blood flow from aorta to a. Pulmonalis, that caused decreased blood in circulation - Right ventricle hypertrophy

  • COARCTATIO AORTA

    Aortic Stenosis left ventricle hypertrophy proximal dilatation, blood >> headache distal vasoconstriction pale of extremity & cold

  • PERICARDIUM

    Fluid in cavum pericardium

    1. HydropericardiumNormal : 30-50cc, serous50cc - D.C, - Chronic kidney disease - Hypoproteinemia chronic pericard adhesion

  • 2. Hemopericardium Blood >> pericardium, because : TraumaRupture of muscle infark myocardrupture of aorta malignant tumorrupture of a. coronary

  • PERICARDITISUsually secundairy of : - hematogen - lymphogen - percontuinitatum Classification of pericardium based of etiology :Tuberculosis pericarditisBacterialis pericarditisRheumatica pericarditis

  • Morphologi : - dilatation of vein & irregularity, ectasion - valves thickening - different of wall thickned - elastic tissue changed by fibrotic

  • Classification of pericardium based of etiology :Tuberculosis pericarditisBacterialis pericarditisRheumatica pericarditisUremic pericarditisVirus pericarditisCarcinomatosa pericarditisMCI because of pericarditisSecundair of : - parasit - fungal Idiopathic

  • Classification from inflammatory exudate : 1. Serousa pericarditis 2. Seurofibrinos pericarditis 3. Fibrinous pericarditis 4. Suppurative pericarditis

  • Pathogenesis1. Heart anomalies MCI Acute rheumatica Surgical trauma

    2.Pulmonary disease Tuberculosis Carcinoma Pneumonia Empyema

  • Complications :Constrictive pericarditisObliterative, focal/diffuse pericarditisV. cava compression -ascites -hepatosplenomegaly4. DC

  • Clinical manifestations : paincongesion & edemastatic dermatitiscellulitischronic ulceration

  • Complications : inflammationperforated of veinthrombosisulceration + dermatitis

  • LymphAcute lymphagitis because of pyogen processChronic lymphagitis because of filariasisNon inflammatory lymphedema because of neoplasmOperative

  • Vessel & Lymph TumorsBenignCapillary HamangiomaTumor capsul (-), vessel proliferation (+), separated by fibrous tissue, ussually at skin & mucosaCavernosum Hemangioma = Cystic hygromaLarge vessel lumen cystic

  • Endothelioma HemangiomaProliferative of endothelPericytoma HemangiomaProliferative of suportive tissue

  • Glomangioma + Glomus TumorSmall, under the skin / nailMalignaAngiosarcoma

  • Kaposis Sarcoma

    Subcutaneus plaque or verucosusIt contains : - endothelial proliferationextravascular hemorrhageanaplastic fibroblast proliferationgranulation like inflammatory reactionVery painfull tumor

  • Virus pericarditisCarcinomatosa pericarditisMCI because of pericarditisSecundair of : - parasit - fungalIdiopathic

  • Terima kasih