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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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