k - 3 & k - 20 penyakit jantung koroner (patologi anatomi)
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PJKTRANSCRIPT
04/21/23 1
BLOOD AND LYMPHATIC VESSEL
Dr.H.Joko S.Lukito, SpPA
Dept. Pathology Anatomy
FK USU
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ARTERYCONGENITAL ABNORMALITIES
Especially aorta & large arteries Generally are assosiated with congenital
heart disease
1. Ascending aorta hypoplasia2. Aortic arch anomalies
- Aorta coarctation- Patent Ductus Arteriosus- Right Subclavian artery posterior- Aortic arch on the right- Double aortic arch
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Degenerative Disease1. Atheroma
2. Arteriosclerosis
Atheroma Normal Arteriosclerosis
Deposition of yellow lipid Tunica intima Generalised
material in plaque under Tunica elastica degeneration
the intima Tunica media media
Tunica adventitia
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Degenerative Disease of the Vessel
Arteries IschaemiaVeins/lymphatic congestive edema
Symptoms :- Functional disorders- Pain, due to :
- Infarction- Trophic disorder- Skin ulceration
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Arteriosclerotic disease
= arterial hardening
Atherosclerotic lipid deposition under the intima
Monckeberg sclerosis calcification on tunica
media Arteriosclerosis in small arteries
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Pathogenesis
1. The developmental of focal areas of chronic endothelial injury
2. Increased insudation of lipoproteins into the vessel wall, mainly LDL or modified LDL with its high cholesterol content
3. A series of cellular interactions in the foci of injury involving ECs, monocytes/ macrophage, T lymphocytes, and SMCs of intimal or medial origin
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4. 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 →
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macrophage and smooth muscle cells -
engulf lipid, macroscopically as fattyfatty
streaks streaks → smooth muscle -prolliferation,
collagen and other ECM deposition , extra
selluler lipid ( so called fibrous cap fibrous cap ) →
fibrofatty atheroma → fibrous plaques
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NORMAL OF BLOOD VESSEL
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ATHEROSCLEROTIC IN BLOOD VESSEL
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Atheroma - Coronary heart disease
- cerebrovascular accident
- extremities gangrene
Major risk factor : Hypertension Cigarette smoking Diabetes
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Minor risk factor : Insufficient reguler physical activity Stress Obesity The use of oral contraceptive Hyperuricemia High carbohydrate intake Hyperhomocysteinemia
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Clinical manifestation caused by ischaemic pain
growth disorder
skin ulceration
Arteriosclerosis complication :
1. Blood vessel occlution
2. Skin ulceration
3. Thrombosis
4. Embolism
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2. Monckeberg sclerosis medial
calsification on tunica media + internal lamina elastica of
arteries grouping Ca sedimentation Aging process
elastic tissue of intima arranged like onion onion skin appearance skin appearance Subintimal hyaline sedimentation.
3. Arteriosclerosis arteriole sclerosis
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INFLAMMATION OF ARTERIESINFLAMMATION OF ARTERIES
1. Acute Infectious Arteritis
Etio : - Perivascular inflammation : acute
meningitis, cellulitis, pneumonia
- Intravascular : septicaemia, septic embolism.
2. Periarteritis nodosa = Polyarteritis = Panarteritis
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Clinical manifestations :- intermitten fever- malaise, lethargy- loss of body weight- peripheral neuritis- myalgia, progressive arthralgia
• Male >> female• At all age• Body organs which are involved : kidney,
brain, heart, skin, lung
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Macroscopic finding :
protruding mass Ø 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
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Periartheritis Nodosa :Periartheritis Nodosa :The ConsequencesThe Consequences
Luminal obliterationThrombosisAneurysmInfarct
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Spesific arteritisSpesific arteritis
1.1. Syphylitic arteritisSyphylitic arteritis
2.2. Tuberculosis arteritis Tuberculosis arteritis with tubercle central necrosis surrounded by lymphocyte cells, epitheloid cells, plasma cells, and Langhans datia cells.
3.3. Rheumatoid arteritis Rheumatoid arteritis – fibrinoid necrosis
4.4. Datia Cells arteritis Datia Cells arteritis = Giant cell arteritis
temporalis arteritis
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Datia Cells Arteritis
Clinical manifestation :
- Fever
- Occurs especially in elders (>50yrs old)
- Temporal, occipital and skull arteries segmental inflamation
- Leucocytosis, BSR increased
- Causes blindnessblindness in chronic inflamation (months)
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Etiology: unknown
Microscopic : - Inflamation reaction on media and internal
elastic lamina of the vessels- Datia cells (+)- Fibrosis of the intima- Thickening of the adventitia
Datia Cells Arteritis
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5. Takayasu disease Takayasu disease = pulseless disease = pulseless disease = Aortic arch syndrome= Aortic arch syndrome
Clinical appearance :
- pulseless diseasepulseless disease
- chronic and progressive
- occurs especially in young women
- visual disturbances
- upper extremities parasthesia
- lethargy (general weakness)-syncope
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Takayasu diseaseTakayasu disease
Microscopic :- pan-arteritis- thickening of the intima- coagulative necrosis- plasma cells , lymphocyte and datia cells
inflitration- fibrosis- perivascular infiltration
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Peripheral Arterial DiseasePeripheral Arterial Disease
I. Arteriosclerosis = arteriosclerosis obliteransArteriosclerosis = 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
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PathologyPathology
- 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.
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2. Raynaud disease2. Raynaud disease
A vasospastic syndrome caused by freezing , restricted on fingers onlyrestricted on fingers only.
Young women
Etiology : blood vessels spasm
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Clinical findings
- distal fingers paleness
- tingling/ numbness and hot
- cyanotic and alternate reddening
- can progress to ichaemic necrotic fingers
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II. Scleroderma = Progressive Systemic Sclerosis
- A systemic disease
- Especially effected the skin
- Fibrosis in the internal organ
- 30-50 years old
- Female >>
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III. Buerger disease III. Buerger disease = Thromboangitis obliterans = Thromboangitis obliterans (Wini Warter ) (Wini Warter )
young male , heavy smokersyoung male , heavy smokers persistent painful legspersistent painful legs, cause by distal
arterial obstruction and occlusion persistent ischemia of 1 or more toes superficial thrombophlebitis
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Macroscopic : Wire like blood vessels (hardening)
Blood vessels occluded by yellow/ grayish
mass due to thrombosis
Perivascular fibrosis
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Microscopic :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
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AneurysmAneurysm
local abnormal dilatation of the artery due to wall defect.
Etiology : - artheriosclerosis- syphilis , bacterial or fungal infection- congenital- trauma
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Clinical form of aneurysm :
- sacculer
- fusiform
- cylindric
- dissecans
- circoid / racemosus
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Favorite localization :
- aortic arch
- abdominal aorta
- popliteal artery
- femoral artery
- carotid artery or subclavia artery
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Complication :
- rupture
- hemorrhage
- compression to other organ
- erosion
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VeinsVeins
Inflamation
Acute phlebitis :
Purulent phlebitis : Abcess, meningitis,
pneumoniaNon Purulent phlebitis : dermatitis,
rheumatoid fever, drug allergy, rheumatoid
arthritis
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Microscopic :
- Inflamation cell infiltration
- oedema
- hyperemia
- blood vessel wall destruction
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Vein Obstruction AbnormalitiesVein Obstruction Abnormalities
1.1. PhlebothrombosisPhlebothrombosis
Vein thrombosis without regional blood vessel destruction.
2.2. ThrombophlebitisThrombophlebitis
Thrombosis cause vessel wall destruction.
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3.3. Vena Cava Superior ObstructionVena Cava Superior Obstruction
due to : bronchogenic Carcinoma
mediastinal lymphoma
Aortic aneurysm
causing : cyanotic and congestion of cephalic v, neck and upper extremities v.
4.4. Vena Cava Inferior ObstructionVena Cava Inferior Obstruction
due to : liver tumor and renal cell Ca.
aneurysm
ascites and inflamation
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5. 5. Portal vein ObstructionPortal vein Obstruction due to : thrombosis
intrahepatic diseases splenectomy polycytemia vera
6. Varicose vein = Varix abnormal vein dilation which restricted due to intraluminal pressure increamentand loss of surrounding tissue support.
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Etio : hereditary weakness vein obstruction intraabdominal pressure >> elderly people standing too much, hard work vein inflammation chronic constipation
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Portal hypertension hemorrhoid
oesophageal varices
Frequently on superficial vein of lower extremities.
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HEART DISEASES
1. Coronary heart disease 1. Coronary heart disease ± 80%± 80%
2. Hipertensive heart disease ± 9%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%
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1. Coronary heart disease
All of myocardium disorders due to a. coronary insuffisience
- arterisclerosis 99%- arterisclerosis 99%
- rheumatica
- sifilis
- arteritis
- polyarteritis
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Variant of coronary heart disease :
1. Arteriosclerotic heart disease
2. Angina pectoris
3. Myocardial infarction
Influenced by :
1. Flow of a. coronary
2. Sensitivity myocardium toward ischaemia
3. O2 concentration of blood
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Condition associated to CHD :
1. Hypertension
2. Obesity
3. Hypercholesterolemia
4. Smoking
5. DM
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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
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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
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Predisposition factors :
1. Lipoprotein serum ↑, soft drink, obesity, alkohol
2. Increased blood pressure
3. Increased blood glucose
4. Stress
5. Lack of exercise
6. Smoking
7. Uric acid serum ↑
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1. Arterioscerotic Heart disease
Arterioscerotic of a. coronary & myocardial fibrosis diffuse & sometimes with valve fibrosis.
Morphologic :
Arterioscerotic muscle ischaemia myocardial fibrosis as diffuse grey plaque …...
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cont’d :myocardium fiber atrophy and contain lipochrom = Brown atrophy so that cor becomes :
small normal swelling (in DC)
Valve abnormalities : mitral valve fibrosis chorda tendinea fibrosis calcification
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Clinical Manifestation :
asymptomaticold age with angina pectorismitral / aortic murmurdamage myocardium on ECGheart congestivearrhythmia and myocardium infarction
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ANGINA PECTORISANGINA 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
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BasicBasic : Myocardium hypoxia due to : coronary arteriosclerosis myocardium luetica polyarthritis nodosa aortic valve insufficience Anemia
Hypoxia caused by : small arteri occlution arteri spasm While exercising paroxysmal myocardium
hypoxia
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MYOCARDIUM INFARCT ( MCI )
Coronary insufficiency due to :
coronary arteriosclerotic 99 % thrombosis and embolismdisease of vesselsnarrowing ostium due to syphilis arteriosclerose and hypotension.
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MCIMCI
Predilection : right a. coronary 40 % left anterior a. coronary 40 % left ventricle
Morphology : Restricted on central myocardium Myocardium : epicardium + endocardium
becomes thick (Ø 3 – 4 cm). Zahn Infarction, subendocardial small lesion
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Myocardium Infarct Progressivity :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 border
6 weeks : fibrosis
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Microscopic :
blood vessel ischaemic → coagulative necrosis in myocardium cell
interstitial edema haemorrhage / haemosiderin pigment neutrophyl exudation fibrosis
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Complication :
Pericarditis fibrinosa / haemorrhagica Mural Thrombosis → embolism Rupture infarction → heart tamponade fibrosis and aneurysm
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Lab :
Nekrosis coagulativa enzyme dehidrogenase ↑glutamic oxaloacetic transaminase ↑
12 – 24 hours• SGOT ↑• Leukositosis ↑• BSR ↑• LDH ↑• C Reactive Protein ↑
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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
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CyanoticHeart arrhythmiaECG : - Q abnormal
- ST elevation - T invertedDeath rate : male >> 2 x female
Incidence : Male : 33- 35 years Female : after menopause
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HYPERTENSIVE HEART DISEASE
Markedly by left ventricle hypertrophy left ventricle hypertrophy due to continous systemic hypertensivesystemic hypertensive.
Incidence : Female >> 2x male Middle age and old age Genetically inherited
Etiology :Hypertensive occur if arterial peripheral resistence ↑
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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
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Muscle hyperthrophy caused by :activity >>→ anoxia myocard
weaknesshypertension → coronary arteriosclerosis
→ myocardium anoxia.hypertension → damage renal blood
vessel → ReninRenin ↑ → NaCl + H2O retention
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Morfology :
left ventricle wall >> ( 2,5 cm )heart weight >>without other heart disordersmicroscopic : normal cardiac musclethickened arterial wall
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Clinical manifestation :
Compensatory stadium : asymptomHypertensive symptom :
headache, palpitation, retinopathyLeft decompensatio cordis :
dyspnoe, cough, hemoptysis
Coronary arteriosclerose symptom
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RHEUMATIC HEART DISEASERHEUMATIC HEART DISEASE
Rheumatic fever is the non supurative systemic inflammation disease. Associated with streptococcus beta streptococcus beta haemolitycus group A haemolitycus group A infection and the immunology reaction with febrile attack and prolonged remission.
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Rheumatic fever is the collagen disease, can occur in :
joint, heart, skin, serous, lung blood vessel
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Incidence : age 5 – 15 years 90 % Low economics Overcrowded area, poor sanitation Low nutrition
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Rheumatic Inflammation Changes:
mucoid degenerationfibrinoid necrosishyaline collagen degeneration
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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 ↑
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Morphology :Specific disorders and pathognomonic :
Aschoff bodyAschoff 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 Ø 1 -4 cmSubcutaneous nodule
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mitral, aortic valve : fibrotic vegetation, calcification
tricuspidale valve : stenosisChorda tendinea : shorten and thicken
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Clinical ManifestationClinical Manifestation :
Major Criteria of Jones:
1. Polyarthritis migrans 85 %
2. Carditis 65 %
3. Chorea sydenham
4. Subcutaneous nodule
5. Erythema marginatum
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Minor Criteria of Jones
1. Leucocytosis
2. BSR ↑
3. ASTO ↑
4. Fever
5. Arthralgia
6. Prolonged PR interval
7. Erythema
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Cause of death :
1. Decompensatio cordis
2. Brain/ renal thromboembolism
3. Bacterial Endocarditis
4. Mitral stenosis
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COR PULMONALECOR PULMONALE
The right ventricle hypertrophy, due to pulmonale disorders :
Etiology :
1.1. AcuteAcute massive pulmonary embolism, so that dilatation right ventricle
2.2. ChronicChronic 1. Pulmonary disease
2. Chronic pulmonary disease
3. Thorax abnormalities
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Ad.1. - Diffuse big/small arteries trombosis
- Embolism
- Diffuse vasculitis
- Fibrosis : - sarcoidosis
- radiation
- asbestosis
- berryliosis
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.Ad.2. - Emphysema
- Chronic bronchitis
- Pulmonary fibrosis due to TBC
- Sarcoidosis
- Severe pneumonia
- Pulmonary resection
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.Ad.3. – Thickness pleura bilateral - Neuro abnormalities :
PoliomyelitisMyasthenia gravisMuscle distrophyKyphoscoliosis
Clinical Manifestation :- dyspnoe - dilatation of vein- oedema - ascites- hydrothorax - hepatosplenomegaly
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CONGENITAL HEART DISEASE
Etiology :
- Unknown
- Genetics
- Infection virus rubella, lues, toxoplasma
- Drug teratogenic thalidomide, cortison, busulfan
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.
1.1. Roger’s diseaseRoger’s 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
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Death because of : - right disease
- endocarditis
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2. Atrium Septal Defect2. Atrium Septal Defect
Over IV weeks
Defect of foramen ovale
Clinically : - cyanotic right sided overload
- hypertrophy right ventricle
- pulmonary hypertension
- systolic murmur
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3. Lutembacher’s disease3. Lutembacher’s disease ASD + Stenosis mitral, right & left
ventricle dilatation, hypertrophy right ventricle
4. Tetralogi Fallot4. Tetralogi Fallota. Defect septum interventricleb. Dextroposed overriding aortac. Stenosis pulmonal valved. Right ventricle hypertrophy
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Clinical manifestation : cyanosis from newborn clubbing of the finger growing disorder
Bad Prognose, cause of death :- Right DC- Endocarditis bacterialis- Brain abcess- Respiratory Tr. Infection
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5. 5. Eisenmenger ComplexEisenmenger 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
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COARCTATIO AORTA
Aortic Stenosis left ventricle hypertrophy proximal dilatation, blood >>
headache distal vasoconstriction pale of
extremity & cold
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PERICARDIUM
Fluid ↓↓ in cavum pericardium
1. HydropericardiumNormal : 30-50cc, serous
50cc - D.C, - Chronic kidney disease
- Hypoproteinemia chronic pericard adhesion
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2. Hemopericardium
Blood >> pericardium, because : TraumaRupture of muscle infark myocardrupture of aorta malignant tumorrupture of a. coronary
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PERICARDITISUsually secundairy of : - hematogen - lymphogen -
percontuinitatum Classification of pericardium based of
etiology :Tuberculosis pericarditisBacterialis pericarditisRheumatica pericarditis
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Morphologi :
- dilatation of vein & irregularity, ectasion
- valves thickening
- different of wall thickned
- elastic tissue changed by fibrotic
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Classification of pericardium based of etiology :
Tuberculosis pericarditisBacterialis pericarditisRheumatica pericarditisUremic pericarditisVirus pericarditisCarcinomatosa pericarditisMCI because of pericarditisSecundair of : - parasit - fungal Idiopathic
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Classification from inflammatory exudate :
1. Serousa pericarditis 2. Seurofibrinos pericarditis
3. Fibrinous pericarditis
4. Suppurative pericarditis
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Pathogenesis
1. Heart anomalies MCI
Acute rheumatica
Surgical trauma
2.Pulmonary disease Tuberculosis
Carcinoma
Pneumonia
Empyema
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Complications :
1. Constrictive pericarditis
2. Obliterative, focal/diffuse pericarditis
3. V. cava compression
- ascites
- hepatosplenomegaly
4. DC
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Clinical manifestations : pain congesion & edema static dermatitis cellulitis chronic ulceration
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Complications : inflammation perforated of vein thrombosis ulceration + dermatitis
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LymphLymphAcute lymphagitis because of pyogen
processChronic lymphagitis because of filariasisNon inflammatory lymphedema because
of neoplasmOperative
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Vessel & Lymph TumorsVessel & Lymph TumorsBenignCapillary HamangiomaTumor capsul (-), vessel proliferation
(+), separated by fibrous tissue, ussually at skin & mucosa
Cavernosum Hemangioma = Cystic hygroma
Large vessel lumen cystic
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Endothelioma HemangiomaProliferative of endothelPericytoma HemangiomaProliferative of suportive tissue
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Glomangioma + Glomus TumorSmall, under the skin / nailMalignaAngiosarcoma
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Kaposi’s SarcomaKaposi’s Sarcoma
Subcutaneus plaque or verucosusIt contains : - endothelial proliferationextravascular hemorrhageanaplastic fibroblast proliferationgranulation like inflammatory reactionVery painfull tumor
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Virus pericarditisCarcinomatosa pericarditisMCI because of pericarditisSecundair of : - parasit - fungalIdiopathic
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