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167 Cards in this Set
- Front
- Back
size of the heart |
300-350 g....50 g less in females |
|
sound upon closure of A-V valves |
S1 |
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Closure of Semilunar valve, Physiologic spitting on inspiration |
S2 |
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Physiologic heart sound in children and young adult, pathologic in those > 40 y/o |
S3 |
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Due to sudden rush of blood in overloaded ventricles |
S3 |
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Best heard at the apex in left lateral decubitus |
S3 |
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Coninsides with a wave, pathologic, due to concentric ventricular hypertrophy (noncompliant ventricle) and volume overloaded ventricle |
S4 |
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Failure of the heart to eject enough blood delivered to it by the venous system to meet the metabolic demands of the body |
CHF |
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Most common admission diagnosis of elderly patient, in often preceeded by cardiac hypertrophy |
CHF |
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Left sided heart failure may be due to |
Systolic dysfunction Diastolic Dysfunction |
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Decreased ventricular Conraction, low EF, e.g. CAD, Post MI, Myocarditis, dilated cardiomyopathy |
Systolic dysfunction |
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Non compliant ventricle, High or normal EF with S4, Concentric LVH due to HPN, restrictive cardiomyopathy, LV overload due to AR, MR |
Diastolic dysfunction |
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Most common manifestation of LHF |
Dysnea |
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Cxr findings in Left side heart failure |
Congestion in Upper lobes (early finding) Perihilar congestion (bat configuration) alveolar infiltrates |
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Right sided heart failure pahogenesis |
Decreased contraction: RV infarct
Non-compliant right ventricle: RVH Increased afterload (pulmonary circulation) : Left sided heart failure, Pulmo hpn Increased preload: TV regurg, L-R Shunt |
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Most common symptom of Right sided heart failure |
Ankle/Pedal and pretibial Edema |
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Chronic passive congestion of the liver can cause |
Nutmeg liver, centrilobular necrosi or cardiac cirrhosis |
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Left sided heart failure in microscopy |
Cardiac myocyte hypertrophy with enlarged peleiotropic nuclie Lungs will show heart failure cells |
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Complications of LHF |
Passive pulmonary congestion and Edema Raas increased causing secondary hyperaldosteronism Cardiogenic shock |
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Most common cause of RVH |
LVH |
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right sided heart failure caused by pulmonary hypertension from intrinsic lung disease |
cor pulmonale |
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RVH presentation |
JVD, Heposplenomegaly, dependent edema, ascites, weight gain, pleural and pericardial effusion |
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High output heart failure |
Beri-beri (Vasodilation of arterioles Anemia (decreased blood viscosity) Hyperthyroidism (Increased SV) Av Fistula: Increase venous return |
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Greatest risk factor of Congenital heart disease |
Congenital heart disease in parent or preceding sibling |
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Top causes of CHD |
VSD ASD PDA TOF |
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MC genetic risk of CHD: |
Down syndrome |
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Most common Cyanotic CHD |
Tetralogy of follow |
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Tetralogy of follow is composed of |
Pulmonic stenosis RVH Overriding the VSD by the aorta VSD |
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Tetralogy of fallot in CXR |
Boot shaped heart |
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Hypoxic spell which improves when squatting |
TET spell |
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Ventriculo-arterial discordance, switching of the aorta and pulmonary arteries |
Transposistion of the great arteries |
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Required shunt for TGA |
VSD (35%) stable shunt PDA (65%) Unstable shunt |
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CXR findings in TGA |
Egg shaped cardiac silloutte |
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TGA is associated with |
Offspring of diabetic mother |
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Closure of the ductus arteriosus occurs due to ____ and when? |
increased O2 saturationi and decreased PGE2 Occurs during first 2 days |
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ductus arteriosus will become |
ligamentum arteriosus |
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Single great artery associated with cyanosis with irreversible HPN Assoc. Shunt |
Truncus arteriosus VSD |
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Complete occlusion of the tricuspid valve (failure of devopment) |
Tricuspid atresia |
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Tricuspid atresia is associated with : |
Hypopastic RV ASD as shunt (right to left) high mortality |
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connection between pulmonary veins and systemic veins wherein blood flow of the pulmo veins goes into the right atrium |
TAPVC |
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MCC variant of TAPVC |
Supracardiac (Drains to inominate/brachiocephalic vien) |
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MC adult CHD- Asymptomatic untill 30 y/o |
ASD |
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Cardiac auscultion finding in ASD |
Fixed widely split S2 with mild systolic murmer of upper sternal border |
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3 types of ASD |
Primum Secundum (90 %) Sinus Venosus |
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Adjcent to AV vavle and usually assoc with cleft anterior mitral, assoc with Downs |
Primum ASD |
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Due to deficient/ Fenestrated oval fossal |
Secundum ASD |
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Near the entrance; commonly accompanied by TAPVC |
Sinus venusos ASD |
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Most common CHD overlall |
VSD |
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Frequently assoc with other structural defects (e.g. Cri du chat, Fetal alcohol syndrome) |
VSD |
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Multiple VSD is called |
Swiss cheese septum |
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Types of VSD |
Membranous (90 %) Infundibular- hole is below pulmonary valve Ventricular septum- Muscular septum |
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PDA is most commonly associated with what type of infection |
Congenital rubella |
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It is the direct communication between the aorta and the pulmonary artery |
PDA |
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Auscultation sound in PDA |
Continuous machinery murmur |
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two forms of Atrioventricular septal defect |
Partial- Primary ASD and cleft anterior mitral leaflet causing mitral insufficiency Complete- hole in the center of the heart: 1 /3 have down syndrome |
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segmental narrowing of the Aorta
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Coarctation of the aorta |
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associated wit turner's syndrome and causes severe narrowing of aorta proximal to the ductus arteriorusus |
Preductal (infantile) Coarctation |
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Causes narrowing distal to the ductus arteriosus |
postductal (adult) Coarctation |
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Symptoms associated with infantile coarctation |
Lower body cyanosis |
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Symptoms associated with adult coarctation |
Upper extremity HPN Rib notching on CXR Possible rupture of berry aneurysm Collateral circulation |
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what CHDs are associated with |
Congenital rubella syndrome- PDA Turner's syndrome- Coarctation (infantile) Down's- ASD primum Marfan's syndrome- MVP, aortic dissection Offspring of diabetic mom- Transposition of the great Arteries |
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infantile Coartation will be associated with what ventricular defect to survive |
PDA RVH |
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What is the cause of rib noching |
Remodeling as a consequence to increased blood flow though the intercostal arteries |
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Complications of adult coarctation could be |
CHF, intracerebral hemorrhage, dissectic aortic aneuryms |
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Coronary vessels supplying the -anterior wall of LV - Anterior ventricular septum - Apex |
LAD |
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MC affected in MI - V1-V4 anterior wall MI |
LAD |
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Coronary vessels supplying the - Inferior/Posterior LV and RV, posterior ventricular septum |
RCA |
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Coranary vessel supplying the lateral wall of LV except apex |
LCX |
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(II, III, AVF, right side chest leads) |
Inferior wall exchemia |
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I, AVL, V5-V6 |
lateral wall ischemia |
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The most common type of ischemia, caused by coronary atherosclerosis with narrowing/stenosis of coronary vessels > 70 % |
Stable angina |
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Chest pain is relieve by rest and nitrates |
Stable |
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Chest pain is relieve by nitrates |
Prinzmetal |
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Chest pain occurs during exertion, excercise due to increase cardiac demand |
Stable |
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Angina pectoris with ST- segment depression ( sub- endochondral ischemia) |
Stable anginga |
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Pre infarction angina |
Unstable/Cresendo angina |
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angina caused by vasospasm due to thromboxane or endothelin |
Prinzmetal angina |
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angina characterised by increasing frequency, intensity, and duration associated with nonocclusive thrombus in an area of atherosclerosis |
Stable/cresendo |
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Death with i hour after onset of SsX secondary to arrhythmia |
Sudden cardiac death |
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SCD associated with what syndromes |
Romano-Ward syndrome ( long QT syndrome -V Fib) Brugada syndrome (RBBB) |
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types of myocardial infarction |
Transmural/Full thickness - ST-elevation, Q wave - Increased early mortality rate -Occured if > 50 % of myocardial wall -associated with regional occlusion by thrombus |
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Types of MI |
Subendocardial - Partial thickness - ST depression - Inner third of myocardium - < 50 % wall involved - Associated with hypoperfusion |
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Changes in MI (gross) |
6- 12 hours- MI usually grossly inapparent 18-24- Pale to cyanotic 1 week- Yellow and softend 7-10 days- Hyperemic granulation at infarct edge 1-2 mos- fibrous scar |
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Irreversible cell injury in MI within how many minutes |
20-40 mins
|
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wavy fibers of myocardium |
within 4 hours |
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Early coagulative necrosis |
4-12 hours |
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Pnemonics in MI 1313 |
1 - 3 days Neutrophils (acute inflammation) 3 - 7 days Macrophages 1 week- granulation tissue 3 weeks- scar |
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Coagulation necrosis with strong neutrophil infiltrates |
> 12 hours |
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ATP reduced to 50 % of normal |
10 minutes |
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Loss of contractility |
2 minutes |
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Microvascular injury |
> 1 hour |
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Reversible phase of MI |
Glycogen depletion, Mitochondrial swelling, relaxation of myofibrils |
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Irreversible phase |
Sarcolemmal disruption, mitochondrial amourphous densities |
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result of calcium overload and hypertetanic contraction after reperfusion of injured myosyte |
Contraction band necrosis |
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Myocardial rupture will most like occur within what days post MI |
3- 7 days -rupture causing tamponade |
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Common 2-3 days post MI |
Dressler syndrome (fibrinous pericarditis) |
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% mortality in cardiogenic shock |
70 % |
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Hypertrophy and dilatation of non-infarted myocardium is called, which can become substrate of aneurysm, secondary arrhytmia |
Cardiac remodelling - prevented by ACE i |
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Preferred biomarkers in MI |
trop I - occurs 2-4 hours - peak at 2 days - disappears at 7 days |
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can diagnose reinfarction |
CKMB - 2-4 hours - peak 24 hours - disappears after 72 hours |
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ECG changes in MI |
Inverted T waves - Correlates with infarct periphery Elevated ST segment- Injured myocardial cells sorrounding necrosis New Q waves- Coagulation of necrosis |
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TReatment of MI |
Antiplatelet (ASA, Clopidogrel)
NItrates, B-blockers, ACE Pain Medications (morphine) - morphine is not used in inferior wall MI Reperfusion therapy |
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Opening snap, loud s1, diastolic rumble, Atrial fib |
MS |
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Due to MVP Pansystolic murmur |
Mitral regurgitation |
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Midsystolic clicks |
MVP |
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Most common cause of congenital aortic stenosis |
Bicuspid valve |
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Widened pulse pressure, austin flint murmur |
Aortic regurgitaion |
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Graham steel murmur |
pulmonary regurgitation |
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IE in drug abusers, carcinoid heart, JVP, pulsating liver, |
tricuspid regurgitation |
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Carcinoid heart disease |
Pulmonary stenosis Tricuspid valve plaques |
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Bounding pulse |
Corrigan water hammer |
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De musst sign |
head nodding with diastole |
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quincke's pulse |
pulsating nail bed |
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Mueller's sign |
systolic pulsation of uvula |
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durosiers |
femoral retrograde bruit |
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traubes sign |
pistol shot femorals |
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hill's sign |
BP LE> BP UE |
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acute, immune mediated, multisystemic inflammatory disease due to pharyngitis from GABHS ( M proteins) |
Rheumatic fever |
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Clinical features |
MAJOR: Joints (migratory Polyarthritis) OH my heart (Carditis) Nodules (subcutaneous) Erythema marginatum Syndenham chorea |
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Diagnosis of RF |
Upon onset of SSx, pharyngeal culture are negative but ASO and Anti-DNAse titers will be positive |
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Pathognomonic of RF and RHD found in all layers of the heart |
Aschoff bodies Anitschow cells |
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Foci of swollen eosinophilic collagen surrounded by T cells, plasma cells |
Aschoff bodies |
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Macrophages containing abundant cytoplasm, round nuclei with slender wavy ribbon of chromatin and aschoff giant cells |
Anitschkow |
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Morphology of RF and RHF |
Bread and butter pericarditis Macculum plaques fibrinoid necrosis Mitral stenosis Fish mouth/ buttonhole stenosis |
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Locations, etiologic agent, valve, prognosis of Infective endocarditis
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Acute IE- Previously normal valve, Tricuspid, Staph aureus, Worse prog, Rapid onset, associated with IV drug use Subacute- Previously abnormal valve, Mitral valve, Strep viridans, Better prog, insiduous onset less destruction, more granulation, RHD |
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Friable, bulky, destructive vegetation with fibrin, inflamatory cells and other organisms in the heart |
infective endocarditis |
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Most common symptom |
Fever |
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Microemboli in IE |
Subungual hemorrhage, jane way, osler's nodes |
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Red linear flame shaped streak on nail beds |
Subungual hemorrhage |
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Red hemorrhage painless lesions on palms and soles |
Jane way |
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subcutaneous nodules in the pulp of digits |
osler's node |
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sterile, non destructive vegetations that may cause emboli along the line of closure of valve leaflets |
Marantic endocarditis |
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Marantic endocarditis commonly occurs in |
Cancer ( mucinous AdenoCA of pancreas and other adenoca Debilitating illness (e.g. renal failure, chronic illness) with DIC Hypercoagulable states |
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Small sterile vegetations on both sides of the leaftlets, with hematoxylin bodies, associated with SLE |
Libman Sakcs disease -resembles fibrosis and may require surgery |
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Small, warty vegetations along the lines of closures of the valve leaflets |
RHD |
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Small bland vegetations, usually attatched at the line of closure |
NBTE |
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Large, irregular masses on the valve cusps that can extend onto the chordae |
IE |
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small or medium sized vegetations on either or both sides of valve leaflets |
LSE |
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Heart disease due to primary abnormality of the myocardium, diagnosed with a bioptome |
Cardiomyopathy |
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Pattern of Cardiomyopathy |
Dilated Hypertrophic Restrictive |
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Characteristic auscultation finding in pericarditis |
Friction rub |
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Type II reaction where necrotic heart muscle induces immune sytem to generate autoantibodies to cardiac self antigen |
Dressler syndrome |
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Most common form of cardiomyopathy, due to enlargement of with dialtation of all four chambers, resulting in progressive CHF |
Dilated cardiomyopathy |
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Some causes of DIlated cardiomyopathy |
IDIOPATHIC Alcohol pregnancy Beri beri Chagas Doxurobucin Cocoine Solvents Chronic anemia |
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LV-EF in the different forms of Cardiomyopathy |
Dilated < 40 % Restrictive >45 - 90 % Hypertrophic > 50 - 80 % |
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Wall description of Cardiomyopathies |
Dilated- thin walls, dilated lumen Hypertrophic- Thick walls, constricted lumen Restrictive- Normal wall and lumen but stiff |
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The only effective therapy for dilated cardiomyopathy is |
Heart transplant |
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also called assymetrical septal hypertrophy, idiopathic hypertrophic subaortic stenosis |
Hypertrophic cardiomyopathy |
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Common cause of deeath in young atlethes due to extensive myocyte hypertrophy with myofiber disarray |
hypertrophic cardiomyopathy |
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Common cause of hypertrophic cardiomyopathy |
Genetic, friedrich ataxia, storage disease, infants with DM mothers |
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Etiologies of restrictive cardiomyopathy |
amyloidosis, sarcoidosis, fibrosis after surgery, loeffler endomyocarditis |
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Right sided endocardial and valvular fibrosis secondary to serotonin, Diagnosis via demonstration of 5 HIAAA |
Carcinoid heart disease |
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Etiology of myocarditis |
Microbes (coxsackie, t. cruzi, B. burgodorferi) RF Toxins (diphteria, co) Drugs ( Coxurobucin, Cocaine SLE, SS, Sarcoidosis |
|
Morphology of myocarditis |
Instertitial inflammatory infiltrate with focal myocyte necrosis |
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Clinical findings in pericardial effusion |
Muffled heart sounds NVE Hypotension with pulsus paradoxus |
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ECG finding in Pericardial effusion CXR |
Electrical alterans Water bottle configuration |
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Follow suppurative or caseaous pericarditis, previous surgery, or irradiation to the mediatinum |
Adhesive mediastinopericarditis |
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Heart sorrounded by fibrous tissue resembling plaster mold usually due to TB or open heart surgery |
Constrictive pericarditis |
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Precordial chest pain, tachycardia, fever, pericardial friction rub |
Pericarditis |
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ECG changes in pericarditis |
Diffuse ST elevation PR Depression |
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Most common Primary tumor of the heart associated with wrecking ball effect on valve, ball-valve obstruction |
Myxoma |
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Heart tumor associated with Tuberous sclerosis |
Cardiac rhabdomyosarcoma |
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Autosomal dominant mutation in TSC1 (hamartin) and TSC2 (tuberin) which are tumor supressor gene |
Tuberous sclerosis |
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MC common heart tumor |
metastasis |
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Most common primary tumor in children |
Rhabdomyosarcoma |
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MC site of metastisis |
pericardium |
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thanks |
thanks |