3714457
Descrição
FlashCards por Jessica Margaux Mercado, atualizado more than 1 year ago
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Criado por Jessica Margaux Mercado
aproximadamente 9 anos atrás
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| Questão | Responda |
| Impaired cardiac function → unable for the cardiac muscles to contract → unable to propel the blood to the systemic circulation → unable to supply oxygen to metabolic processes | Congestive Heart Failure |
| Pathophysiologic state resulting from impaired cardiac function that renders the heart muscle unable to maintain an output sufficient for the metabolic requirements of the tissues & organs | Congestive Heart Failure |
| In order to maintain the CO, the heart muscles must stretch → dilatation of the heart muscles → increase in the preload and increase in the contractility of the heart → increased cardiac output (volume pumped out). | Frank – Starling Mechanism |
| Increased cross-sectional areas of the myocytes; increase wall thickness , reduced cavity diameter | Pressure overload or Concentric hypertrophy |
| deposition of new sarcomeres; cell length and width and muscle mass and wall thickness are increased in proportion to chamber diameter | Volume overload |
| CHF: Fetal gene program | c-fos, c-myc, c-jun, EGR1 |
| Mechanism: direct impairment of myocardial contractility (CHF) | Myocardial Dysfunction: IHD, Dilated CMP |
| Mechanism: excessive pressure (CHF) | Ventricular Overload; HPN, AS, PE, cor pulmonale |
| Mechanism: excessive volume (CHF) | Ventricular Overload; Aortic Regurgitation, Mitral Regurgitation |
| Mechanism: high output states (CHF) | Ventricular Overload: pregnancy, anemia, thyrotoxicosis |
| Mechanism: reduced myocardial expansion (CHF) | Restrictive disease Myocardial :Restrictive/ Ischemic CMP, amyloidosis, myocarditis Pericardial : pericarditis, tamponade |
| Mechanism: disrupted electrical function (CHF) | Electrical disorders: Pathological tachycardia, heart block |
| Mechanism: unknown (CHF) | Iatrogenic: Drugs : doxyrubicin, cocaine ; Radiation |
| Mechanism: electrical conduction disruption (CHF) | Conduction System Failure: AMI Arrhythmia |
| Mechanism: Inflammation, Degenerative, Congenital (CHF) | Valvular Failure: Endocarditis, RHD, Calcific Aortic Stenosis, Pulmonary Stenosis, Tricuspid Atresia |
| Mechanism: Congenital (CHF) | Cardiac Malformation: VSD, ASD, PDA, Tetralogy of Fallot, Coarctation of Aorta |
| CHF: Impaired contractile function → dec CO; S/S: pulmonary congestion; progressive deterioration of myocardial contractile function | Systolic Dysfunction; IHD, HPN, Dilated CM, pressure/volume overload |
| CHF: reduced ventricular compliance; Inability of the heart to relax and expand → dec ventricular filling → dec CO | Diastolic Dysfunction: Massive LV hypertrophy, amyloidosis, constrictive pericarditis, myocardial fibrosis |
| Left-Sided Heart Diseases | IHD, MI, HPN, Aortic/Mitral Valve Disease, Non-ischemic Myocardial Disease |
| Pulmonary congestion, edema; Peripheral edema, hypoxic encephalopathy | Left-sided Heart Failure |
| dyspnea, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea , tachy, cardiomegaly, blood-tinged sputum, cyanosis, rales | Left-sided Heart Failure |
| Causes: pulmonary embolism, intrinsic lung disease (COPD, cystic fibrosis), pulmonary HPN, kyphoscoliosis, pneumoconiosis, schistosomiasis | Right-Sided Heart Failure |
| Mechanism: Increased pulmonary vascular resistance due to fibrosis and/or hypoxic vascular response | Right-Sided Heart Failure |
| CPC of liver, centrilobular necrosis, sclerosis; congestive splenomegaly, congestion in kidneys, hypoxic encephalopathy, ascites, pleural effusion, edema | Right-Sided Heart Failure |
| splanchnic congestion: hepato-splenomegaly, hepatojugular reflex, jugular venous distention, dependent edema, transudative effusions (ascites, pleural effusion), cyanosis | Right-Sided Heart Failure |
| heart failure secondary to pumping excessive volume of blood | High-Output Failure |
| High-Output Failure: causes | Anemia, Hyperthyrodism, high fever, arteriovenous shunts |
| Secondary to ischemic heart disease (IHD), hypertension, dilated cardiomyopathy, and vulvar/pericardial disease | Low-Output Failure |
| CRITERIA FOR DX OF CHF: Major Criteria | PND, Neck vein distention, Rales, Cardiomegaly, Acute pulmonary edema, S3 gallop, inc venous pressure, hepatojugular reflux |
| CRITERIA FOR DX OF CHF: Minor Criteria | dependent edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, vital capacity reduced by 1/3 from normal, tachycardia (>120 bpm) |
| imbalance between blood supply/perfusion to the heart and its demand for oxygenated blood; limits oxygenation, ATP generation, reduces availability of nutrients and removal of metabolic wastes | Myocardial ischemia |
| Syndromes: AMI, angina pectoris, chronic ischemic heart disease, sudden cardiac death | IHD |
| dec coronary artery perfusion relative to myocardial demand; chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, variable degrees of superimposed acute plaque change, thrombosis, and vasospasm | IHD |
| 70% of lumen of one or more CA is/are obstructed with atherosclerotic plaque; compensatory CA vasodilatation is insufficient to meet moderate increases in myocardial O2 demand | Critical stenosis |
| acute plaque changes | fissure, rupture, ulceration, hemorrhage |
| myocardial infarct where the whole wall of the muscle has undergone cell death | acute transmural MI |
| Paroxysmal, recurrent precordial or substernal chest pain, caused by transient (15s to 15min) myocardial ischemia that falls short of infarction | Angina pectoris |
| chest pain: transient (<15 min), precipitated by exertion and emotion, relieved by rest, vasodilators | Stable/Typical Angina Pectoris |
| Episodic, recurrent chest pain at rest; caused by coronary artery spasm; ECG: suggestive of transmural ischemia (ST segment elevation); responds promptly to vasodilators | Prinzmetal or variant AP |
| 90% vessel block; pain progressiveljy increasing in frequency, duration (>15 min), intensity, occurs at rest | Unstable or crescendo AP; pre-infarction AP, crescendo AP, Q-wave AP |
| local coagulative necrosis of myocardium due to ischemia; irreversible damage to myocardium | ACUTE MYOCARDIAL INFARCTION |
| Severe Ischemia 20-40 mins. or longer + <10% blood flow + initial damage to sarcolemma membrane | Irreversible Myocardial Damage |
| Pathognomonic sign: ischemic coagulative necrosis; central damage at subendocardium progresses into transmural in a waveform fashion | Myocardial Infarction |
| involves >2/3 or full thickness of ventricular wall; ischemia due to superimposed thrombus in atherosclerosis (chronic obstruction + acute plaque change + complete thrombosis) | TRANSMURAL: STEMI |
| inner 1/3 or 1/2 of ventricular wall; ischemia due to dec blood volume (e.g. hypovolemic shock, hypotension, diffuse stenosing coronary artery atherosclerosis w/o thrombosis and acute plaque change) | SUB-ENDOCARDIAL: NSTEMI |
| triphenyl tetrazolium chloride: unstained pale zone (due to the lactate dehydrogenase leakage that follows cell death) | Infarct |
| S/S: hypotension, rapid weak pulse, diaphoretic & nauseous, dyspnea; ECG: ST elevation, new Q waves, T wave inversion | MI |
| progressive heart failure as a consequence of ischemic myocardial damage → fibrosis → reduce cardiac activity → ischemia | Chronic IHD; Ischemic CM |
| Gross: left ventricular dilation and hypertrophy, often with discrete areas of gray-white scarring; moderate to severe atherosclerosis; Histo: diffuse subendocardial myocyte vacuolization, fibrosis from previous infarction | Chronic IHD |
| SA node damaged → AV node takes over | Bradycardia |
| atrial dilation → irritable atrial myocytes →independent & sporadic depolarization of each atrial myocytes → variable signal transmission to AV node | Atrial fibrillation |
| dysfunctional AV node: inc PR interval on ECG | 1st degree heart block |
| dysfunctional AV node: intermittent signal transmission | 2nd degree heart block |
| dysfunctional AV node: complete failure | 3rd degree heart block |
| S/S: palpitations, lightheadedness, syncope, sudden cardiac death | Arrhythmia |
| adaptive response to pressure overload on the heart that can lead to myocardial dysfunction, cardiac dilatation, CHF and in some cases sudden death | SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE |
| Concentric left ventricular hypertrophy in the absence of other cardiovascular pathology that might induce cardiac hypertrophy | SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE |
| Gross: thickened left ventricular wall (concentric), cardiomegaly, decreased luminal size; Histo: inc transverse diameter of the myocytes, boxcar nuclei, intercellular fibrosis | SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE |
| pressure overload in the right ventricle due to increased pulmonary resistance usually caused by chronic lung disease that can lead to pulmonary vasculature fibrosis | PULMONARY (RIGHT-SIDED) HYPERTENSIVE HEART DISEASE |
| right ventricular dilatation after massive pulmonary embolization | Acute Cor Pulmonale |
| right ventricular (and often right atrial) hypertrophy; result of chronic RV pressure overload; seen in COPD, CRPD, long standing pulmonary artery disease, chest wall motion impairment | Chronic Cor Pulmonale |
| Gross: marked RV dilation without hypertrophy | Acute Cor Pulmonale |
| Gross: RV wall thickens and RV dilation may lead to tricuspid regurgitation | Chronic Cor Pulmonale |
| heart disease resulting from a primary abnormality in the myocardium; attributed to intrinsic myocardial disease | Cardiomyopathy |
| biventricular and bi-atrial dilatation; hypo-contracting heart muscle; systolic dysfunction; low LV ejection fraction, low CO = congestion | DILATED (CONGESTIVE) CARDIOMYOPATHY |
| Causes: idiopathic, previous viral myocarditis, alcohol or other toxic exposure, peripartum cardiomyopathy/pregnancy, genetic causes, iron overload | DILATED (CONGESTIVE) CARDIOMYOPATHY |
| cardiomegalic heart, global enlargement, generalized chamber dilatation, annular ring dilatation, valvular defects, functional regurgitation, mural thrombus | DILATED (CONGESTIVE) CARDIOMYOPATHY |
| ages of 20-50, slowly progressive CHF, including dyspnea, easy fatigability, poor exertional capacity; secondary mitral regurgitation and abnormal cardiac rhythms are common, and embolism from intracardiac (mural) thrombi | DILATED (CONGESTIVE) CARDIOMYOPATHY |
| Idiopathic Hypertrophic Subaortic Stenosis (IHSS), Hypertrophic Obstructive CM, Asymmetric Septal Hypertrophy | HYPERTROPHIC CARDIOMYOPATHY |
| myocardial hypertrophy in the interventricular septum w/o ventricular dilatation, abnormal diastolic filling and LV outflow obstruction; heavy, muscular, hypercontracting heart | HYPERTROPHIC CARDIOMYOPATHY |
| missense mutation in sarcomere (B-MHC gene); inc myofilament activation = myocyte hypercontractility | HYPERTROPHIC CARDIOMYOPATHY |
| Asymmetric septal hypertrophy → outflow obstruction; septal wall ratio >1.3; massive myocardial hypertrophy w/o ventricular dilatation; banana-like ventricular cavity | HYPERTROPHIC CARDIOMYOPATHY |
| Impaired diastolic filling of the massively hypertrophied LV; dec CO and increase in pulmonary venous pressure -> exertional dyspnea with harsh systolic ejection murmur | HYPERTROPHIC CARDIOMYOPATHY |
| Gross: non-dilated ventricular chamber; bi-atrial dilatation due to poor ventricular filling and pressure overload; Histo: patchy or diffuse interstitial fibrosis, identifiable depositions/infiltrations | RESTRICTIVE (INFILTRATIVE) CARDIOMYOPATHY |
| Dense diffuse fibrosis of ventricular endocardium and subendocardium, often involving the tricuspid and mitral that extends from the apex upward; linked to nutritional deficiencies and/or inflammation related to helminthic infections | Endomyocardial fibrosis |
| Hypereosinophilia and eosinophilic tissue infiltrates, endomyocardial fibrosis, large mural thrombosis | Loeffler endomyocarditis |
| Focal or diffuse thickening usually involving the mural LV endocardium; heart is infiltrated by fibroelastic tissue | Endocardial fibroelastosis |
| Inherited disease; defective cell adhesion proteins in desmosomes that link adjacent myocytes; right ventricular failure and rhythm disturbances (particularly ventricular tachycardia or fibrillation) with sudden death | ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY |
| Disorder characterized by arrhythmogenic right ventricular cardiomyopathy and hyperkeratosis of plantar palmar skin surfaces | Naxon Syndrome |
| RV wall: severely thinned because of loss of myocytes, extensive fatty infiltration and fibrosis | ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY |
| infectious agents and/or inflammatory processes primarily target the myocardium; result in injury to cardiac myocytes (necrosis and degeneration) not typical of ischemic heart disease | MYOCARDITIS |
| Gross: beefy red myocardium due to vascular congestion; ventricular myocardium is flabby and mottled by either pale foci or minute hemorrhagic lesions | MYOCARDITIS |
| Histo: interstitial inflammatory myocardial necrosis near the inflammatory cells; vascular congestion, edema; viral inclusions and parasitic organisms may be present | MYOCARDITIS |
| edema, interstitial inflammatory infiltrates, and myocyte injury; diffuse lymphocytic infiltrate; self-limiting | Acute Viral Myocarditis |
| presence of multi-nucleated giant cells; infiltrates: Lymphocytes, eosinophils, necrosis, patchy myocitic necrosis in muscle cell | Fiedler’s Myocarditis; Giant Cell Myocarditis |
| Interstitial infiltrate: macrophages, a lot of eosinophils with little or no necrosis; no granulomas; associated with adverse drugs effects of methyldopa | Hypersensitivity Myocarditis |
| ASD, VSD, PDA, AVSD; acyanotic, right ventricular hypertrophy and eventually failure | LEFT-TO-RIGHT SHUNT ANOMALIES |
| early cyanosis; hypertrophic osteoarthropathy, polycythemia, paradoxical embolization; Tetralogy of Fallot, Transposition of Great Vessels, Truncus Arteriosus, Tricuspid Atresia, TAPVR | RIGHT-TO-LEFT SHUNT ANOMALIES |
| untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis | Eisenmenger syndrome |
| Basic defect: Abnormal opening at the level of the atrial septum; most common CHD that is asymptomatic until adulthood; S/S may manifest in 3rd decade | ATRIAL SEPTAL DEFECT |
| 90% of ASD ; defect in the fossa ovale | Secundum ASD |
| defect occurs (low-lying) near the AV valve; associated with a clefted anterior mitral valve/ abnormal tricuspid valve | Primum ASD |
| Located at the top, near the entrance of SVC; associated with total anomalous pulmonary venous return to the right atriu | Sinus Venosus Defect |
| Located in the upper portion of the interventricular septum; affects membranous portion | Membranous VSD |
| VSD: located below the pulmonary valve | Infundibular VSD |
| VSD: found in the muscular wall of the interventricular septum | Muscular VSD |
| Presence of holes in the atrial and the ventricular level; abnormal development of atrio-ventricular canal; incomplete closure of AV septum and inadequate formation of the tricuspid valve and mitral valve | ATRIO-VENTRICULAR SEPTAL DEFECT (AVSD) |
| Failure of fusion of superior and inferior endocardial cushions with the mid portion of the atrial septum and the muscular (trabecular) portion of the ventricular septum | ATRIO-VENTRICULAR SEPTAL DEFECT |
| primum atrial septal defect and a cleft in the mitral valve | Partial AVSD |
| Defects of both the primum atrial septum and inlet ventricular septum and the presence of a common atrioventricular valve; free communication of all 4 chambers | Complete AVSD |
| AVSD: mitral and tricuspid annuli are separate; usually associated with a primum ASD | Partial/Incomplete AVSD |
| AVSD: single atrioventricular valve annulus; defect of the inlet ventricular septum | Complete AVSD |
| Persistence of communication between the aorta (a high pressure chamber) and the pulmonary artery (a relatively low pressure chamber) via a non-closure of the ductus arteriosus | Patent Ductus Arteriosus |
| continuous, harsh murmur: “Machinery murmur” | Patent Ductus Arteriosus |
| inability of the great vessel to rotate to its normal location | Tetralogy of Fallot |
| VSD; subpulmonic stenosis (right ventricular outflow tract obstruction); overriding of the VSD by the aorta; right ventricular hypertrophy | Tetralogy of Fallot |
| Heart is large and “boot-shaped” as a consequence of right ventricular hypertrophy; proximal aorta is dilated; hypoplastic pulmonary trunk | Tetralogy of Fallot |
| Hemodynamic consequences: R-to-L shunting, dec pulmonary blood flow, inc aortic volume; polycythemia w/ attendant hyperviscosity and hypertrophic osteoarthropathy | Tetralogy of Fallot |
| with good APGAR score (pink complexion, without cyanosis); mild pulmonary stenosis; may present with L→R shunt | Pink tetralogyPink tetralogy |
| severe pulmonary stenosis, greater resistance to right ventricular outflow, R→L shunt (blood cannot go to the lungs → cyanotic) | Classic tetralogy |
| Abnormal formation of the truncal and aortopulmonary septa | Transposition of the Great Arteries |
| ventrico-aterial discordance: aorta from RV, PA from LV; RV Hypertrophy, LV Hypoplasia/Atrophy | Transposition of the Great Arteries |
| failure of separation of truncus arteriosus into aorta and pulmonary artery; single great artery or a single great vessel that receives blood from both ventricles | Patent Truncus Arteriosus |
| Complete absence of the development of the tricuspid valve; cyanosis is present virtually from birth; blood cannot flow into the right ventricle | Tricuspid Atresia |
| results from unequal division of AV canal; mitral valve is larger than normal and almost always underdevelopment (hypoplasia) of RV | Tricuspid Atresia |
| Pulmonary veins do not drain into left atrium, but into left innominate vein or coronary sinus | TAPVR |
| Results embryologically when the common pulmonary vein fails to develop or becomes atretic; needs PFO or VSD | TAPVR |
| common pulmonary vein fails to develop or becomes atretic; right atrial and ventricular dilatation, pulmonary trunk dilation , hypoplastic left atrium | TAPVR |
| Tubular hyperplasia of aortic arch proximal to Patent Ductus Arteriosus (PDA) | INFANTILE COARCTATION |
| Circumferential narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus; leads to the inc of pressure in the pulmonary trunk proximal to the obstruction | INFANTILE COARCTATION |
| Ridge-like coarctation of aorta at the level of or after ligamentum arteriosus; aortic arch and its vessels are dilated and presence of LVH | ADULT COARCTATION |
| disparity in the blood pressure of the upper extremities (increased) and of the lower extremities (decreased) | Coarctation of the Aorta |
| pulmonary artery and valve becomes tight and stenotic; patient presents with a sinus disorder | PULMONARY STENOSIS AND ATRESIA |
| Narrowing/obstruction of aortic valve at the level of the valve | Valvular Aortic Stenosis |
| Narrowing/obstruction of aortic valve below the aorta | Subaortic Stenosis |
| Narrowing/obstruction of aortic valve above the aorta | Supravalvular Stenosis |
| Failure of valve to open completely, impeding forward flow | Stenosis |
| Failure of valve to close completely, leading to reversal of flow of blood | Insufficiency/regurgitation |
| No anatomic defect in the valve; dilated cardiomyopathy – the ventricular chambers dilate → annular ring dilates → annular ring cannot close completely → regurgitation of blood from ventricle to atrium | Functional regurgitation |
| Most often caused by age-related “wear and tear"; involves the aortic valve which becomes obstructed by the calcium deposits at the roof of the valve | Calcific Aortic Stenosis |
| Heaped calcified masses within aortic cusps; protrudes into the sinuses of Valsalva, mechanically impeding valve opening; no commissural fusion | Calcific Aortic Stenosis |
| Unequal sized bicuspid valve with midline “raphe”; only two valvular leaflets | Congenital Bicuspid Aortic Valve Stenosis |
| Calcific nodular deposits in the annular ring; common in elderly women with myxomatous mitral valve, or mitral valve prolapse | Mitral Annular Calcification |
| Irregular, stony hard nodules behind the mitral valve leaflets; ballooning of the mitral leaflets; affected leaflets are enlarged, redundant, thick, and rubbery; tendinous cords also tend to be elongated, thinned, and occasionally rupture | Mitral Annular Calcification |
| Thinning of the valve layer known as the fibrosa layer of the valve; middle spongiosa layer expands, owing to increased deposition of myxomatous (mucoid) material | Mitral Annular Calcification |
| auscultatory finding caused by abrupt tension on the redundant valve leaflets at chordae tendinae as the valve attempts to close | Midsystolic click (Mitral Annular Calcification) |
| Colonization of heart valves and mural endocardium by microbiologic agents, forming bulky vegetations; most common valves involved are mitral and aortic | Infective Endocarditis |
| Fibrin deposits on injured endothelium; circulating bacteria are trapped by the forming thrombus, infecting the microthrombi (hematogenous seeding) | Infective Endocarditis |
| Highly virulent organism; arises in normal valve; necrotizing, ulcerative and destructive lesions; bulky, friable vegetations; more severe clinical signs and symptoms, higher morbidity | ACUTE INFECTIVE ENDOCARDITIS |
| occurs in previously diseased valve; low virulent organism; insidious clinical onset | SUBACUTE INFECTIVE ENDOCARDITIS |
| . Irregular reddish tan vegetations overlie valve cusps; Fever, weight loss, fatigue, anorexia, changing murmurs, embolic phenomenom: Roth spots, sub-ungal hemorrhages, CVA, embolic infarcts, focal/diffuse GN, abscesses | INFECTIVE ENDOCARDITIS |
| Sterile vegetations; associated with debilitated patients, carcinoma, sepsis, and cachexia; nondestructive | NONBACTERIAL THROMBOTIC ENDOCARDITIS; Marantic endocarditis |
| Valvular damage is not a prerequisite for NBTE; usually found on previously normal valves; hypercoagulable states are the precursor | NONBACTERIAL THROMBOTIC ENDOCARDITIS |
| Small nodules along lines of closure, may be bulky & friable, single or multiple, leaflets often normal; free of inflammation | NONBACTERIAL THROMBOTIC ENDOCARDITIS |
| Associated with SLE; affects MV and TV; sterile, small vegetations located in the under-surface of cords | LIBMAN-SACKS ENDOCARDITIS (ENDOCARDITIS OF SYSTEMIC LUPUS ERYTHEMATOSUS) |
| finely grandular, fibrinous eosinophilic material containing "hematoxylin bodies"; • Intense valvulitis may be present characterized by fibrinoid necrosis of valve | LIBMAN-SACKS ENDOCARDITIS |
| Caused by carcinoid tumors which secrete vasoactive amines; neuroendocrine tumor; Clinical findings: episodic skin flushing, cramps, nausea, vomiting and diarrhea | CARCINOID HEART DISEASE |
| Distinctive, glistening white intimal plaque-like endocardial fibrous thickening on the inside surfaces of the cardiac chambers and both TV and PV; tricuspid insufficiency and pulmonic stenosis | CARCINOID HEART DISEASE |
| Minor Criteria: migratory polyarthritis, carditis, subcutaneous nodules, erythema marginatum, Sydenham's cholera (St. Vitus "Dance") | RHEUMATIC FEVER |
| Minor Criteria: fever, arthralgia, Hx of sore throat, inc anti-steptolysin O, inc acute phase reactants: ESR, CR | RHEUMATIC FEVER |
| Central zone of degenerating, hyper-eosinophilic extracellular matrix infiltrated by lymphocytes, plasma cells, and plump activated macrophages | Aschoff bodies |
| plump activated macrophages ; pathognomonic for RF | Anitschkow monocytes |
| Diffuse inflammation and Aschoff bodies may be found in any of the 3 heart layers | Caterpillar cells |
| irregular thickenings, usually in the LA; subendocardial fibrosis | Mac Callum plaques |
| Verruccal necrotic vegetations on lines of closure, Aschoff bodies, Anitschkow monocytes, Caterpillar cells, Mac Callum plaques | RF/RHD |
| Latent period (20-30 years) before symptoms appear; Multi-valvular | RF/RHD |
| Fish mouth deformity; commissural fusion of cusps -> stenosis/regurgitation; deformity or "buttonhole" stenosis (typically affecting MV) and regurgitaion | RF/RHD |
| Leaflet thickening, commissural fusion and shortening, and thickening and fusion of the chordae tendinae; fibrosis & subendocardial fibrosis | RF/RHD |
| large and bulky lesions on the valve cusps that can extend onto the chordae | Infective Endocarditis |
| small, warty vegetations along the lines of closure of the valve leaflets | RHD |
| small, bland vegetations usually attached at the line of closure | NBTE |
| big and small, up and down (both sides of valve leaflets) vegetations | LSE |
| Most common form of valvular disease in industrialized countries; 20-40 ages, females; MV are enlarged, hooded or floppy; developmental anomaly of connective tissue from a dense collagen to a myxoid tissue | MITRAL VALVE PROLAPSE; MYXOMATOUS VALVE PROLAPSE |
| Myxomatous degeneration; where one or more mitral valve leaflets are “floppy” and prolapse into the LA during systole (because of hooding of valve) | MITRAL VALVE PROLAPSE; MYXOMATOUS VALVE PROLAPSE |
| Interchondrial ballooning (hooding) of the mitral leaflets, prolapse into the atrium; leaflets are enlarged, redundant, thick and rubbery; tendinous cords: elongated, thinned, or even ruptured and the annulus is dilated | MITRAL VALVE PROLAPSE; MYXOMATOUS VALVE PROLAPSE |
| Mid-systolic click (snapping and tensing of everted cusp) | ACUTE PERICARDITIS |
| Characteristically produced by non infectious inflammatory diseases; Scanty Inflammation; May or may not cause pericardial serous effusion | Serous Pericarditis |
| Causes of Serious Pericarditis | o Rheumatic Heart Disease o SLE o Scleroderma o Tumors o Uremia o Viral |
| Composed of serous fluid variably admixed with fibrous exudate | Serofibrinous Pericarditis |
| Reflects an active infection caused by microbial invasion; Frank infection leads to systemic symptoms: Spiking fevers and rigors; Organization by scarring is the usual outcome | Purulent or Suppurative Pericarditis |
| Exudate composed of blood mixed with fibrinous or suppurative effusion | Hemorrhagic Pericarditis |
| Most commonly caused by the spread of malignant neoplasm to the pericardial space; In persons with bleeding diathesis; Often follows cardiac surgery | Hemorrhagic Pericarditis |
| Pericardial involvement occurs by direct spread from TB foci within the tracheobronchial nodes; Common antecedent of fibrocalcific, chronic constrictive pericarditis; Epitheloid granuloma with Langhan’s giant cell surrounded by PMN inflammation | Caseous Pericarditis |
| Obliteration of the pericardial sac with adhesion to parietal pericardium that strains cardiac function; S/S: Sytolic retraction of the rib cage and diaphragm, pulsus paradoxus | ADHESIVE MEDIASTINOPERCARDITTIS |
| organization merely produces plaque-like fibrous thickenings | soldier’s plaque |
| Obliteration of the pericardial sac with encasement of the heart in a dense, fibrous or fibrocalcific scar that limits diastolic expansion and cardiac output | CONSTRICTIVE PERICARDITIS |
| Extreme cases can resemble plaster mold (concretio cordis); dense enclosing scar, cardiac hypertrophy and dilation cannot occur; S/S: distant or muffled heart sounds, elevated jugular venous pulse, peripheral edema | CONSTRICTIVE PERICARDITIS |
| most common primary cardiac tumor in adults; benign neoplasm from primitive multipotent mesenchymal cells | Myxoma |
| GNAS1 | McCune-Albright Syndrome (Encoding of G-protein subunit) |
| PRKAR1A | Carney Complex (Encoding of cyclic-AMP dependent protein kinase) |
| Region of the fossa ovalis (favored site of origin); sessile or pedunculated masses; vary from globular hard masses, mottled with hemorrhage to soft, transluscent, papillary, or villous lesions having gelatinous appearance | Myxoma |
| most common primary cardiac tumor in children; commonly discovered in the first years of life; most arise from obstruction of a valvular orifice or ventricular chamber | Rhabdomyoma |
| large rounded, or polygonal cells with cytoplasmic glycogen vacuoles | Spider cells |
| Vacuoles are separated by strands of cytoplasm running from the plasma membrane to the more or less centrally located nucleus | Rhabdomyoma |
| TSC1 and TSC 2 are absent = myocyte growth | tuberous sclerosis-associated rhabdomyomas |
| often regress spontaneously, they may be considered as hamartomas rather than true neoplasms | Rhabdomyoma |
| inhibits mTOR | TSC proteins TSC1: Hamartin TSC2: Tuberin |
| Localized, well circumscribed, benign tumors, mature fat cells, occurs in subendocardium, subepicardium, or myocardiuml; most often located in left ventricle, right atrium, or atrial septum | Lipoma |
| Nonneoplastic deposition of fat in the atrial septum | lipomatous hypertrophy |
| Lesions include white and brown adipose tissue and small interspersed areas of myocardium | Lipoma |
| Curious, usually incidental, sea-anemone-like lesions; resembles Lambl excresences that represents remotely organized thrombus on the aortic valves of older individuals | PAPILLARY FIBROELASTOMA |
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