CARDIOVASCULAR PATHOLOGY - PowerPoint PPT Presentation

1 / 46
About This Presentation
Title:

CARDIOVASCULAR PATHOLOGY

Description:

Endocarditis of systemic lupus. erythematosis (SLE) Carcinoid heart disease ... Systemic lupus erythematosus. Drug hypersensitivity (e.g., methyldopa, sulfonamides) ... – PowerPoint PPT presentation

Number of Views:4440
Avg rating:5.0/5.0
Slides: 47
Provided by: Luer
Category:

less

Transcript and Presenter's Notes

Title: CARDIOVASCULAR PATHOLOGY


1
CARDIOVASCULAR PATHOLOGY
  • Tutorial II
  • William H. Luer M.D.

2
TOPICS
  • Endocarditis
  • Myocarditis
  • Pericardial disease

3
ENDOCARDITISCAUSES
  • Rheumatic fever (covered in lecture)
  • Infection
  • Non-infective
  • Nonbacterial thrombotic endocarditis
  • Endocarditis of systemic lupus
  • erythematosis (SLE)
  • Carcinoid heart disease

4
INFECTIVE ENDOCARDITIS
  • Definition the infection of the endocardium
    (esp. heart valves) by a microbiological agent,
    with the formation of thrombotic debris and
    organisms known as vegetations.

5
INFECTIVE ENDOCARDITIS CAUSES
  • Bacteria, most common
  • Fungi
  • Rickettsiae (Q fever)
  • Chlamydiae

6
CAUSES OF BACTERIAL ENDOCARDITIS
  • Alpha-hemolytic streptococci esp. with damaged
    or otherwise abnormal native valves
  • Staphylococcus aureus healthy or deformed
    valves, esp. in intravenous drug abusers
  • Coagulase-negative staphylococci esp. with
    prosthetic valves
  • HACEK group Haemophilus, Actinobacillus,
    Cardiobacterium, Eikenella, Kingella
    (commensals of oral cavity)
  • Gram-negative bacilli

7
PREDISPOSING FACTORS FOR INFECTIVE ENDOCARDITIS
  • Rheumatic heart disease
  • Myxomatous mitral valve
  • Calcific valvular stenosis
  • Bicuspid aortic valve
  • Artificial (prosthetic) valve (but may develop on
    previously normal valve)

8
PREDISPOSING FACTORS (CONT.)
  • Neutropenia
  • Immunodeficiency
  • Therapeutic immunosuppression
  • Diabetes mellitus
  • Alcohol or IV drug abuse
  • Sepsis
  • Invasive procedures

9
PATHOLOGY OF INFECTIVE ENDOCARDITIS
  • Vegetations of fibrin, inflammatory cells,
    bacteria or other organisms
  • Vegetations located most commonly on heart
    valves, esp. aortic mitral
  • Vegetations may erode perforate valve, may
    erode into underlying myocardium to produce an
    abscess (ring abscess)
  • Vegetation may produce emboli that produce septic
    infarcts in brain, kidney, myocardium, other
    organs

10
Vegetation
Stick in Perforation
Mitral Valve
Infective endocarditis with perforation of
mitral valve leaflet
11
Microscopic View of Vegetation of Endocarditis,
Fibrin Inflammatory Cells
12
CLINICAL FEATURES OF INFECTIVE ENDOCARDITIS
  • Fever, chills
  • Fatigue, weight loss, flu-like syndrome
  • Murmur (may change as vegetation and/or damage to
    valve changes)
  • Petechiae

13
COMPLICATIONS OF INFECTIVE ENDOCARDITIS
  • Valvular insufficiency or stenosis with resulting
    congestive heart failure
  • Myocardial ring abscess
  • Suppurative pericarditis
  • Septic infarcts abscesses
  • Focal diffuse glomerulonephritis

14
NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE)
  • Definition The deposition of sterile
    vegetations on the leaflets of cardiac valves,
    also called MARANTIC ENDOCARDITIS

15
NBTE PATHOLOGY
  • Vegetations of fibrin, platelets, other blood
    elements (i.e.. a thrombus)
  • Vegetations are sterile, nondestructive,
    noninflammatory small (1-5mm)
  • Vegetations occur singly or multiply along the
    lines of closure of heart valves

16
NBTE PATHOGENESIS
  • Probably occurs as a consequence of a
    hypercoagulable state
  • Seem with concomitant venous thrombosis /or
    pulmonary embolism
  • May be seen with hyperestrogenic state, extensive
    burns, or endocardial trauma from indwelling
    catheters

17
NBTE CLINICAL
  • Local effect on valve unimportant
  • May produce emboli with resultant infarcts
  • May eventually organize leaving delicate strands
    of fibrous tissue

18
ENDOCARDITIS OF SLE
  • Also known as Libman-Sacks endocarditis
  • Small sterile vegetations on mitral tricuspid
    valves or fibrous thickenings occurring with the
    antiphospholipid syndrome
  • Circulating antiphospholipid antibodies also
    associated with venous or arterial thrombosis,
    recurrent pregnancy loss, and thrombocytopenia

19
PATHOLOGY OF SLE ENDOCARDITIS
  • Vegetations are small (1-4 mm), single or
    multiple, sterile, granular, and pink
  • Frequently located on the undersurfaces of AV
    valves, but may be elsewhere on valves or even on
    mural endocardium of atria or ventricles
  • Vegetations consist of finely granular fibrinous
    eosinophilic material
  • May have valvulitis, characterized by fibrinous
    necrosis, contiguous with vegetation
  • Can result in fibrosis and valve deformity that
    can resemble chronic rheumatic heart disease

20
CARCINOID HEART DISEASE (CarHD)
  • Seen in one half of patients with carcinoid
    syndrome (episodic skin flushing, cramps, nausea,
    vomiting, and diarrhea)
  • Involves endocardium and valves of the right side
    of the heart

21
CarHD PATHOLOGY
  • Intimal thickenings on the inside surfaces of the
    cardiac chambers valvular leaflets, mainly on
    the right side of the heart
  • Thickenings consist of smooth muscle cells
    sparse collagen fibers embedded in an acid
    mucopolysaccharide rich matrix that expands the
    endocardium
  • Underlying structure of the heart intact

22
CarHD PATHOPHYSIOLOGY
  • Carcinoid tumors produce a variety of bioactive
    products including serotonin, kallikrein,
    bradykinin, histamine, prostaglandins,
    tachykinins
  • Serotonin appears to induce the cardiac lesions

23
CarHD LOCATION
  • Lesions are usually right sided since serotonin
    inactivated by pulmonary vascular endothelial
    monoamine oxidase
  • Can see left sided lesions if have high levels of
    serotonin not completely inactivated by lungs,
    pulmonary carcinoid, or right to left cardiac
    shunts

24
CARCINOID-LIKE HEART LESIONS
  • Left sided lesions can be seen with methysergide
    or ergotamine treatment for migraine headache
    since these serotonin analogs are metabolized to
    serotonin by lungs
  • Left sided lesions can be seen with fenfluramine
    phemtermine (fen-phen) appetite suppressants
    since they affect serotonin metabolism

25
MYOCARDITIS
  • Definition inflammatory processes of the
    myocardium that result in injury to the cardiac
    myocytes.

26
CAUSES OF MYOCARDITIS INFECTIONS
  • Viruses (e.g., coxsackie, ECHO, HIV)
  • Chlamydia (e.g., C. psittaci)
  • Rickettsiae (e.g., R. typhi)
  • Bacteria (e.g., C. diphtheria)
  • Fungi (e.g., Candida)
  • Protozoa (e.g., toxoplasmosis)
  • Helminths (e.g., trichinosis)

27
CAUSES OF MYOCARDITIS IMMUNE-MEDIATED
  • Postviral
  • Poststreptococcal (rheumatic fever)
  • Systemic lupus erythematosus
  • Drug hypersensitivity (e.g., methyldopa,
    sulfonamides)
  • Transplant rejection

28
CAUSES OF MYOCARDITIS OTHER
  • Sarcoidosis
  • Giant cell myocarditis

29
MYOCARDITIS GROSS PATHOLOGY
  • Heart may appear normal or dilated, some
    hypertrophy may be present
  • Ventricular myocardium may be flabby and mottled
    by pale foci and/or minute hemorrhage foci
  • May have mural thrombi

30
MYOCARDITIS MICROSCOPIC PATHOLOGY
  • Interstitial inflammatory infiltrate, may be
    patchy, most commonly have mononuclear cell
    infiltrate, predominantly lymphocytes
  • Focal necrosis
  • Hypersensitivity myocarditis has lymphocytes,
    macrophages, eosinophils
  • Giant cell myocarditis has multinucleated giant
    cells with lymphocytes, eosinophils, plasma
    cells, macrophages with necrosis

31
MYOCARDITIS MICROSCOPIC PATHOLOGY (cont.)
  • Healing myocarditis results in fibrosis
  • Chagas disease has parasitization of myofibers by
    Trypanosomes with neutrophils, lymphocytes,
    macrophages, and eosinophils

32
MYOCARDITIS CLINICAL
  • Fatigue, dyspnea, palpitations, precordial chest
    pain, fever
  • Can be asymptomatic
  • Heart failure, dilated cardiomyopathy
  • Arrhythmias
  • Mitral regurgitation
  • Can result in sudden death

33
PERICARDIAL DISEASE
  • Pericardial effusion
  • Pericardial hemorrhage
  • Pericarditis

34
PERICARDIAL EFFUSION
  • Distention of pericardial sac by transudate
  • Causes include infection, autoimmune disease,
    congestive heart failure, renal failure,
    malignancy, myocardial infarction, drugs, and
    radiation
  • Clinically may see low blood pressure, dyspnea,
    dizziness, and chest pain
  • If fluid compresses heart get cardiac tamponade
    with severe decrease in cardiac output

35
PERICARDIAL HEMORRHAGE
  • Bleeding into the pericardial sac
  • Causes include cardiac rupture from myocardial
    infarction or perforating trauma and ruptured
    aortic dissection
  • May produce compression of the heart with
    resulting cardiac tamponade

36
PERICARDITIS TYPES
  • Serous pericarditis
  • Fibrinous serofibrinous pericarditis
  • Purulent or suppurative pericarditis
  • Hemorrhagic pericarditis
  • Caseous pericarditis
  • Adhesive mediastinopericarditis
  • Constrictive pericarditis

37
PERICARDITIS CAUSES
  • Infections
  • Rheumatic fever
  • Autoimmune disease
  • Drug reaction
  • Myocardial infarction
  • Uremia
  • Malignancy
  • Radiation

38
SEROUS PERICARDITIS
  • Characteristically produced by noninfectious
    inflammations (e.g. rheumatic fever, SLE,
    scleroderma, tumors, uremia)
  • May be produced by adjacent infection (e.g.
    bacterial pleuritis)
  • Microscopically see inflammatory reaction in
    epicardium and pericardium with PMNs,
    lymphocytes, and histiocytes
  • Slow leakage of fluid of high specific gravity
    rich protein content into pericardial sac, (about
    50-200 ml)

39
FIBRINOUS SEROFIBRINOUS PERICARDITIS
  • Most frequent types of pericarditis
  • Composed of serous fluid mixed with a fibrinous
    exudate
  • Common causes include acute myocardial
    infarction, uremia, radiation, rheumatic fever,
    SLE, trauma, postinfarction syndrome

40
FIBRINOUS SEROFIBRINOUS PERICARDITIS (CONT)
  • In fibrinous pericarditis, have finely granular
    pericardial surface may produce a pericardial
    friction rub
  • In serofibrinous pericarditis, inflammation leads
    to leakage of fluid inflammatory cells into
    pericardial sac in addition to fibrin
  • Fibrin may be digested or organize

41
Granular Visceral Pericardial
Surface of Fibrinous Pericarditis
42
PURULENT OR SUPPURATIVE PERICARDITIS
  • Pus in pericardial sac usually from infective
    organisms
  • Acute inflammatory reaction involving pericardium
    with purulent exudate
  • If survive usually organizes, may produce
    constrictive pericarditis

43
HEMORRHAGIC PERICARDITIS
  • Blood mixed with fibrin or pus
  • Can be seen with tuberculosis and other bacterial
    infections, malignancy, and following cardiac
    surgery

44
CASEOUS PERICARDITIS
  • Usually due to tuberculosis
  • Caseous granulomatosis inflammation involves the
    pericardium
  • May lead to fibrocalcific chronic constrictive
    pericarditis

45
ADHESIVE MEDIASTINOPERICARDITIS
  • May follow suppurative or caseous pericarditis,
    cardiac surgery, or mediastinal radiation
  • Pericardial sac obliterated adherence of the
    outer portion of the parietal pericardium to
    surrounding structures produces great stain on
    cardiac function
  • Increased work on heart leads to cardiac
    hypertrophy and dilatation

46
CONSTRICTIVE PERICARDITIS
  • May follow suppurative, hemorrhagic, or caseous
    pericarditis
  • Pericardial sac obliterated heart surrounded by
    dense adherent layer of scar tissue with or
    without calcification (if extreme encasement
    called concretio cordis)
  • Encasing scar limits diastolic expansion of heart
    leading to decreased cardiac output
Write a Comment
User Comments (0)
About PowerShow.com