Cvs146 Slide Cardiovasculer

8/8/2019 Cvs146 Slide Cardiovasculer

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CARDIOVASCULER

Dr.H.Delyuzar Sp.PA (K)


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ISCHAEMIC HEART DIASEASE (80%)

HYPERTENSIVE HEART DIASEASE ( 9%)

HEARTRHEUMATIC HEART DIASEASE ( 2-3 %)

DISEASECONGENITAL HEART DIASEASE (2 %)

-

SYPHILLIS HEART DIASEASE ( 1%)

COR PULMONALE DIASEASE ( 1 %)

OTHERS ( 5%)2


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CORONARY HEART DISEASE


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ARTERIOSCLEROTIC ANGINA PECTORIS MYOCARDIAL

8/24/20104 Departemen Pathology Anatomy - Cardiovascular


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ARTERIOSCLEROTIC HEART DISEASE

Atherosclerotic coronary artery

Diffuse myocardial fibrotic occasionally cardiac valvefibrotic

MORPHOLOGY

Atherosclerotic Ischaemic Myocardial fibrotic

Marked as

Brownish-yellow granular diffusely (accumulates in the heart

Brown Atrophy

muscle) contained lipofuscin (complexes of lipid & protein)



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ARTERIOSCLEROTIC HEART DISEASE

The heart is become:

Small Normal

Enlarged

Disorder of cardiac valve :

Mitral valve fibrotic

C or ae ten ineae i rotic or ca ci ication



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Gross appearance of heavily fibrotic andl ifi d di lalcified cardiac valve



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Intermittent chest pain caused by transient, reversible myocardialischaemic

PRINZMETAL / UNSTABLEANGINA PECTORIS VARIANT,

ANGINAANGINA PECTORIS

(cressendo angina )



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Po ularl called heart attack

Develo ment of an area of m ocardial necrosis caused b localischaemia

Coronary atherosclerosis (99%)

Coroner insufficiency caused by :

Vascular diseases

Osteum occlusion caused by syphillis

Arteriosclerosis occlusion &

Hypotension



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a ogenes s

Severe coronary atherosclerosis Acute atherosclerotic plaque change (rupture)

uper mpose p ete et act vat on Thrombosis & vasospasm

Consequence:

M ocardial Res onse

Cessation of aerobic glycolysis anaerobic glycolysis Inadequate product of phosphate (Creatine phos & ATP)


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Distribution of infarcts

Ri ht coronar Left anteriorartery

(30-40 %)descending artery

(40-50 %)

Left circumflexartery

(15-20 %)



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8/24/2010Departemen Pathology Anatomy - Cardiovascular17


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Evolution Of Morphologic Changes in Myocardial

Infarction

Time Gross Feature Light Microscopic

Findin s

Electron

Microsco ic

Findings

Reversible Injury

< hr None None Relaxation of myofibrils; glycogenloss; mitochondrial

swellingIrreversible Injury

-4 hr None Usually none; variablewaviness of fibers at

Sacrolemmaldisruption;

border mitochondrialamorphous densities

4 -12 hr Occasionally dark Beginning coagulation; ;

haemorrhage



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Evolution Of Morphologic Changes in Myocardial

Time Gross Feature Light Microscopic Findings

Infarction

r ar mo ng oagu a on necros s; con rac on

band necrosis at periphery ofinfarct; neutrophilic infiltrate

- -- -myofibers; heavy neutrophilicinfiltrate

3 - 7 da s H eremic border; central ellow-tan Be innin disinte ration of deadsoftening myofibers, with dying neutrophils;

early phagocytosis of dead cells bymacrophages at infarct border

7 - 10 days Maximally yellow-tan & soft, withdepressed red-tan margins

Well-developed phagocytosis ofdead cells; early formation offibrovascular granulation tissue at



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Time Gross Feature Light Microscopic Findings

10 - 14 days Red-gray depressed infarct borders Well-established granulation tissuewith new blood vessels & collagen

deposition

2 8 wk Gray-white scar, progressive fromborder toward core of infarct

Increase collagen deposition, withdecreased cellularity

> 2 month Scarring complete Dense collagenous scar



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HYPERTENSIVE HEART DISEASE


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Morphology

Concentric hypertrophy (symetric, circumferential> 450 gm)

Size:

ar y: orma ate

Microscopic

Myocytes >

Nuclei: large, hyperchrom, boxcar shaped



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Rheumatic Fever may cause

Chronic valvularHD in acute phase

cute r eumat c car t s

Only 3% group A streptococcal pharyngitis RF

Initial reactivation with subsequent pharyngeal infections

Ab >< M protein cross reaction with glycoprotein :

earJoints & others

Onset : 2-3 weeks after infection Streptococci (-) in lesion8/24/201030 Departemen Pathology Anatomy - Cardiovascular


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Morphology

Inflammator infiltrates in : Synovium Joint Skin Heart (most importantly) fibrosis deformities Lung

Initial tissue reaction : focal fibrinoid necrosis



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Acute Rheumatic Carditis (ARC)

Characteristic :

Inflammatory in 3 layers of heart (Pancarditis)

Hallmark of ARC : (Aschoff bodies)

Multiple foci of inflammation within connective tissue of heartentra ocus i rinoi necrosisSurrounded by : Mononucleous

Anitschkow cells(large histiocyte, vesicular nuclei, abundant basophilic cytoplasm)



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Endocardium

Valvular inflammation tends to : mitral & aortic valves

e va ve pre sposes :

Small vegetations (valve closure) = verrucous endocarditis



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Infective Endocarditis

Infection of the cardiac valve /mural surface of the endocardium

thrombotic (debris+organism) [term vegetation]

Caused by bacteria

Acute Sub-acute

Previously abnormal valve

(Staph. Aureus)

ow v ru ence

(-Hemolytic Streptococcus)



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ege a ons :

Bacteria or other organism Sin le / multi le

May involved : > 1 valve

Most common : Aortic & Mitra

RV valve drug abuser

Fungal



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Bacteriemia

Etiology IV Drug Abuse

Dental Sur er

Catheter Brushung teeth

Risk Preexisting cardiac abnormal

Prosthetic heart valvesI V drug abuser

8/24/201042Departemen Pathology Anatomy - Cardiovascular


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Virus, o enic bacteria, m cobacteria, fun i

Cause :

Secondary to :

Acute myocard infarct Cardiac surgery

Radiation to the mediastinum

Uremia RF, SLE, metastatic malignancies



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er car s may :

1. Immediate hemodynamic complications-.

3. Progress to chronic fibrosing process



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Morphology

Acute pericarditis

Patients with uremia / acute RF : fibrinous, shaggy (bread& butter pericarditis)

Viral : fibrinous

Acute Bacterial : fibrinopurulent

Tuberculous : caseous

Metastases : shaggy fibrinous

Acute fibrinous / fibrinopurulent resolve, sequelae (-)



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Com lications

1. Constrictive ericarditis

2. Obliterate pericarditis (Focally / diffuse)

3. V. Cava compression, causes : Ascites

Hepatosphlenomegaly

.

8/24/201049

Departemen Pathology Anatomy - Cardiovascular


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Pericardial Effusions

Serous Serosanguineous Chylous

CvHDHypoalbumiemia

Blunt chest traumaMalignancy

Mediastinallymphatic

obstruction

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Hemopericardium

Separately from hemorrhagic pericardium effusion

Pure blood :

Ruptured aortic aneurisma

Ruptured myocar infarct

cardiac tamponade death

8/24/201051



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In the region of the foramen

ova e on t e interatria

septum is a small atrial septaldefect as seen in this heartopened on the right side.Here the defect is not closedy e sep um secun um, so

a shunt exists across fromleft to right.


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Congenital Heart Diseaseongenital Heart Disease Type of Defect Mechanism Ventricular Septal Defect (VSD) There is a hole

within the membranous or muscular portions of the intraventricular septum thatpro uces a e t-to-rig t s unt, more severe wit arger e ects

Atrial Septal Defect (ASD) A hole from a septum secundum or septum primumdefect in the interatrial septum produces a modest left-to-right shunt

Patent Ductus Arteriosus PDA The ductus arteriosus, which normall closes soonafter birth, remains open, and a left-to-right shunt develops

Tetralogy of Fallot Pulmonic stenosis results in right ventricular hypertrophy and aright-to-left shunt across a VSD, which also has an overriding aorta

pulmonic trunk from the left ventricle. A VSD, or ASD with PDA, is needed forextrauterine survival. There is right-to-left shunting.

Truncus ArteriosusThere is incomplete separation of the aortic and pulmonaryoutflows alon with VSD which allows mixin of ox enated and deox enated bloodand right-to-left shunting Hypoplastic Left Heart SyndromeThere are varyingdegrees of hypoplasia or atresia of the aortic and mitral valves, along with a small toabsent left ventricular chamber

Coarctation of Aorta Either ust roximal infantile form or ust distal adult formto the ductus is a narrowing of the aortic lumen, leading to outflow obstruction

Total Anomalous Pulmonary Venous Return (TAPVR) The pulmonary veins do

not directly connect to the left atrium, but drain into left innominate vein, coronarysinus, or some other site, leading to possible mixing of blood and right-sided overload


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Here is a heart with both an atrial

ventricular septal defect (VSD). Theheart is opened on the left side.Such small defects do not roducesignificant left-to-right shunting, butthey do increase the risk for

infective endocarditis.


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The aorta is opened longitudinally here

to reveal a coarctation. In the re ion ofthe narrowing, there was increased

turbulence that led to increasedatherosclerosis.

from a patient with a coarctation. Theaorta narrows postductally here toabout a 3 mm o enin .


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The diagram above depicts the findings with a persistent

truncus arteriosus.

This occurs when there is failure offusion and descent of the s iralridges of the truncus and conus that

would ordinarily divide into aortaand pulmonic trunck respectively.

completely descend, the aortic andpulmonic trunks are left undividedat their outflow.

e runcus overr es oventricles.

The persistent truncus is alwaysaccompanied by a membranousventricular septal defect.

This diagram depicts the features of Tetralogy of


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This diagram depicts the features of Tetralogy of

Fallot

.

2. Overriding aorta;

3. Pulmonic stenosis;

. g ven r cu arhypertrophy.

The obstruction to right ventricularoutflow creates a ri ht-to-left shunt that

leads to cyanosis.


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In the diagram above, transposition of


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g , p

e rea vesse s s s own. This occurs when the trunco-conal

.Instead, it descends straight down.

As a result, the outflow of rightventricle is into the aorta and theoutflow from the left ventricle isinto the pulmonic trunk.In orderfor this system to work, there must

e a connec on e ween e sys emand pulmonic circulations.Sometimes this is through a

septal defect. In the diagram at theleft, this is through a patent ductusarteriosus.


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Cvs146 Slide Cardiovasculer

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