Warning:
JavaScript is turned OFF. None of the links on this page will work until it is reactivated.
If you need help turning JavaScript On, click here.
The Concept Map you are trying to access has information related to:
Primary Heart Disease, PERICARDITIS -mostly 2ndary -Primary usually VIRAL Healed Organization->plaques or adhesions or ->obliteration of sac ->adhesive pericarditis -both rarely restrict cardiac action BUT Adhesive Mediastinopericarditis-restricts -can ->hypertrophy, mimic DCM -after surgery, XRT, supp/caseous Constrictive-encased in SCAR -mimics restrictive CM-limit diastole -can have calcifications ->concretio cordis (like plaster mold) HYPERTROPHY/DILATION CAN'T OCCUR -diff'ate from adhesive MSP -QUIET heart Tx-remove fibrous shell, Primary Heart Disease NEOPLASIA Primary Tumors Rare -Mets in 5% of dying CA pts -myxomas>fibromas>lipomas> pap fibroelastomas>angiosarcomas -all BENIGN, 80-90% of primary, HYPERTROPHIC CM (HCM) - DIASTOLIC D/O (idiopathic hypertrophic subAo stenosis) (hypertrophic obstructive CM) -myocard hypertrophy, abnl diastolic filling, 1/3 w/ intermittent LV outflow obstruction -HEAVY, MUSCULAR, HYPERCONTRACTING heart MORPHOLOGY-massive hypertrophy w/out dilation -disproportionate thickening of septum vs. LV free wall -asymmetric septal hypertrophy (10% symmetric) -banana-shaped ventricle->obstructed LV outflow -endocardial thickening, mural plaque formation, thickening of mitral valve leaflet -HUGE myocyte diameter -haphazard array of bundles, myocytes, sarcomeres -interstitial/replacement fibrosis DISTINGUISH from amyloidosis, HTN-caused hypertrophy PATHOGENESIS-1/2 familial-AUTO DOMINANT -mutations in 1 of 4 sarcomere genes -beta-myosin heavy chain MOST FREQUENT -esp 403 Arg->Gln->sudden death -troponin T, tropomyosin, myosin-BP C CLINICAL-impaired diastolic filling b/c no space in LV -DOE due to outflow obstruction, secondary high pulm VP -harsh systolic ejection murmur -focal myocardial ischemia -A FIB w/ MURAL THROMBUS, EMBOLIZATION, infx endocarditis of mitral, cardiac failure, death -SUDDEN UNEXPLAINED DEATH IN YOUNG ATHLETES -heterogeneous presentation TX to enhance LV relaxation-removal of mm Known Causes Hyperthyroidism-tachycardia, palpitations, cardiomegaly, supravent arrhythmias -cardiac failure usually w/ other cardac dz -looks like nonspecific hypertrophy, Primary Tumors Rare -Mets in 5% of dying CA pts -myxomas>fibromas>lipomas> pap fibroelastomas>angiosarcomas -all BENIGN, 80-90% of primary Others Lipoma-MOSTLY LV, LA, atrial septum -in subendo, subepi, myocardium ->ball-valve obstruction Papillary Fibroelastoma-usually incidental -on valves on origination side -hairlike projections -covered by endoth w/ myxoid under -may be organized thrombi -like LAMBL EXCRESCENCES on Ao Rhabdomyoma-MOST FREQ OF KIDS -obstruct valve orifice, or chamber MORPH-SPIDER CELLS -high freq of TUBEROUS SCLEROSIS Angiosarcomas just like elsewhere, DILATED CARDIOMYOPATHY(DCM) (Congestive CM) FLABBY, HYPOCONTRACTING heart -90% of CMs -progressive hypertrophy, dilation, SYSTOLIC dysfcn Causes: Myocarditis-Coxsackie-virus B nucleic acids Alcohol or other toxicity-nutritional or EtOH -acetaldehyde is esp toxic -Thiamine def->beriberi heart dz (like DCM) -DOXORUBICIN -Cobalt Pregnancy-ass'd-Peripartum CM -late pregnancy or wks-mos postpartum -could be due to preg-HTN, volume overload, nutritional def, other Genetic-20-30% familial-all inheritances -dystrophin, oxphos, beta-oxidation mutations Idiopathic-most others-unknown etiology MORPHOLOGY-heart wt=2-3x NL, large, flabby -dilation of all chambers->thins walls ->mural thrombi->emboli ->mitral, tricuspic regurg -no cor aa. dysfcn -interstitial, endocardial fibrosis present -small subendocardial scars -due to ischemic necrosis from low perfusion CLINICAL-any age, esp 20-60yo -slowly progressing CHF -could go from compensated to decomp -End Stage w/ EF=25%-5 yr mort=75% -Death due to progressive cardiac failure, arrhythm -embolism may occur -Arrhythmogenic RV CM/dysplasia->sudden death -due to fatty infiltrate from loss of myocytes Known Causes Doxyrubicin (Adriamycin) - CTX agent -also daunorubicin ->dose-dependent DCM -due to lipid peroxidation of myofiber membranes ->myofiber swelling, vacuolization, fatty change Others:Lithium, Phenothiazines, Chloroquine, Cocaine ->mycard injury->death Tx-discontinue offending agent->quick resolution -can leave fibrosis or scars-look like DCM Cyclophosphamide (Cytoxan) can-> CM after 1 hgih dose! -vascular dmg->myocardial hemorrhage, PERICARDITIS -mostly 2ndary -Primary usually VIRAL Acute Fibrinous/Serofibrinous-MOST FREQUENT -serous fluid w/ fibrinous exudate -CAUSES-acute MI, Dressler syndrome, uremia, chest radiation, RF, SLE, trauma, surgery MORPH-F-dry w/ fine granular roughening SF-more/thicker fluid, yellow/cloudy(RBCs, WBCs, fibrin[can become organized]) CLINICAL-LOUD RUB, pain, fever, c. failure signs -rub quieter w/ serous Serous-usually noninfx inflamm -RF, SLE, scleroderma, tumors, uremia -infx contiguous to pericardium may->serous -sometimes viral (young adults)-w/ myocarditis -MORPH-scant PMNs, lymphos, histios -slow accum of little fluid -if inflam of pericard fat - chronic pericarditis, Primary Heart Disease NEOPLASIA Radiation ->pericarditis, pericard effusion, myocardial fibrosis, ->accel cor aa. dz, mural/valvular fibrosis CA->NBTE, carcinoid ht dz, amyloid, pheochromocytoma-ass'd myocard dmg CTX Complications, Primary Heart Disease Myocardial Disease-Cardiomyopathy -Primary in myocard -3 clinical, fcnal, pathologic pictures DILATED CARDIOMYOPATHY(DCM) (Congestive CM) FLABBY, HYPOCONTRACTING heart -90% of CMs -progressive hypertrophy, dilation, SYSTOLIC dysfcn Causes: Myocarditis-Coxsackie-virus B nucleic acids Alcohol or other toxicity-nutritional or EtOH -acetaldehyde is esp toxic -Thiamine def->beriberi heart dz (like DCM) -DOXORUBICIN -Cobalt Pregnancy-ass'd-Peripartum CM -late pregnancy or wks-mos postpartum -could be due to preg-HTN, volume overload, nutritional def, other Genetic-20-30% familial-all inheritances -dystrophin, oxphos, beta-oxidation mutations Idiopathic-most others-unknown etiology MORPHOLOGY-heart wt=2-3x NL, large, flabby -dilation of all chambers->thins walls ->mural thrombi->emboli ->mitral, tricuspic regurg -no cor aa. dysfcn -interstitial, endocardial fibrosis present -small subendocardial scars -due to ischemic necrosis from low perfusion CLINICAL-any age, esp 20-60yo -slowly progressing CHF -could go from compensated to decomp -End Stage w/ EF=25%-5 yr mort=75% -Death due to progressive cardiac failure, arrhythm -embolism may occur -Arrhythmogenic RV CM/dysplasia->sudden death -due to fatty infiltrate from loss of myocytes, Primary Heart Disease Pericardial Disease PERICARDITIS -mostly 2ndary -Primary usually VIRAL, Primary Heart Disease Myocardial Disease-Cardiomyopathy -Primary in myocard -3 clinical, fcnal, pathologic pictures RESTRICTIVE CM -primary decrease in vent. compliance ->implaired diastolic filling -but contractile fcn unaffected -idiopathic or ass'd w/ other myocard dzs -radiation fibrosis, amyloidosis, sarcoidosis, tumor mets, inborn errors of metabolism Dx via endomyocardial Bx MORPHOLOGY-ventricles ~NL to slightly enlarged -cavities not dilated, firm myocardium -biatrial dilation -patchy, diffuse interstitial fibrosis (min. to extensive) -w/ known causes, similar grossly, different uscopically Other Restrictive conditions: -Endomyocardial Fibrosis-children-young adults in Africa -fibrosis of vent endocard, subendocard -Apex -> T/M valves ->dim'd volume, compliance->mural thrombi -Loeffler Endomyocarditis-sim to above, not geographic -often eosinophilia, eosinophilic leukemia -often abnl cells, release MBP->endocard dmg ->scarring, thrombotic layering->poor prognosis -Endocardial Fibroelastosis-focal or diffuse thickening -mural LV endocardium -in first 2 years of life, uncommon in adults -focal can be (-)Sx, diffuse deadly in kids