Pathology 2 - Block 2 - Part 2

davidwurbel7's version from 2016-06-16 16:13

Valvular Heart Disease Part 2

Question Answer
Characterized by formation of bulky, friable,easily detached and infected vegetations. Vegetations destroy the valve leaflet and Chordae tendineaeEndocarditis
Caused by highly virulent organisms e.g. S. aureus. Affected valve rapidly destroyed. Difficult to cure with antibiotics alone; often require surgical interventionAcute Infective Endocarditis
Caused by less virulent organisms e.g.Strep. viridans. Leads to insidious infections of previously damaged valvesSubacute Infective Endocarditis
Acute infective endocarditis is more likely caused by this organismS. aureus
Subacute infective endocarditis is more likely caused by this organismS viridans
Prior to Dental and surgical procedures, Urinary catheterization and GI endoscopy, this should be done to prevent infective endocarditisProphylactic Antibiotic
MC overall cause of IEStreptococcus viridans
2nd MC overall cause of IEStaph. aureus
MCC of IE in IVDAStaph. aureus
MC cause of IE after prosthetic valveStaph. epidermidis
MC cause of IE from intravenous cathetersStaph. epidermidis
MC cause of IE in ulcerative colitis or colorectal cancerStrep. bovis
Hemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella produce this type of endocarditis in which signs and symptoms suggest infective endocarditis. However, organisms cannot be isolatedCulture Negative Infective Endocarditis
Bacteria that is the second MCC of infective endocarditis in IVDAPseudomonas
The most common overall valve involved in IEMitral Valve
The most common valve involved with IVDATricuspid Valve
Symptoms include systemic - Fever, chills, weakness, rigors, weight loss; Cardiac - dyspnea, chest pain, clubbing. Regurgitant murmur (new onset or increased intensity), Signs of CHF, Retinal hemorrhage with pale center and Hematuria and RBC casts. Splinter hemorrhages in nail beds. Osler’s node (painful) on pads of fingers and toes. Janeway lesions painless hemorrhagic lesions on hand and feet Infective Endocarditis
Retinal hemorrhage with pale centerRoth's Spot
Painful lesions on pads of fingers and toes due to microembolizationOsler's Nodes
Painless hemorrhagic lesions on hand and feetJaneway Lesions
Endocarditis with large, sterile vegatations that have a tendency to embolizeNon-Bacterial Thrombotic Endocarditis
Endocarditis with large, infected vegatations that have a tendency to embolizeInfective Endocarditis
Endocarditis with small, sterile vegatations with the vegatations located at the lines closureRheumatic Fever
Endocarditis with small, sterile vegatations with areas of fibrinoid necrosis that do not have a tendency to embolize. The vegatations can be located all over the valveLibman-Sacks Endocarditis
Libman-Sacks Endocarditis is associated with this conditionSLE

Congenital Heart Diseases

Question Answer
Abnormalities/malformations of the heart or great vessels that are present at birthCongenital Heart Defect
The most common congenital heart defect is thisVentricular Septal Defect
Congenital heart disease associated with Turner's SyndromeCoarctation of Aorta
Congenital heart disease associated with congenital rubella infectionPatent Ductus Arterosis
Left to right shunts are termed thisAcyanotic CHD
Right to left shunts are termed thisCyanotic CHD
O2 from 75% to ~80% in right side.Step-up Shunt
O2 from 95% to ~80% in left heart Step-down Shunt
This shunt cause volume overload in the right side of the heartLeft-Right Shunt
Complications of this shunt includes pulmonary hypertension, RVH due to pulmonary HT. Eventually, reversal of shunt (Eisenmenger’s syndrome). Occurs when right ventricular pressure overrides left ventricular pressures. Patient develops cyanosisLeft-Right Shunt
Shunt reversal when right ventricular pressure overrides left ventricular pressuresEisenmenger’s Syndrome
Oxygen saturation results: RA o ; RV + ; PA + ; LA o ; LV o ; AO oVSD
Oxygen saturation results: RA + ; RV + ; PA + ; LA o ; LV o ; AO oASD
Oxygen saturation results: RA o ; RV o ; PA + ; LA o ; LV o ; AO oPDA
This part of the interventricular septum is most commonly involved in a VSDMembranous Ventricular Septum
A large VSD most likely occurred in this part of the interventricular septumMembranous Ventricular Septum
A small VSD most likely occurred in this part of the interventricular septumMuscular Ventricular Septum
Cri du chat syndrome, trisomy 13 and trisomy 18 and Fetal alcohol syndrome have association of this cardiac abnormalityVSD
Most common CHD to be diagnosed in adult lifeASD
Ostium secundum defectPatent Foramen Ovale
CHD associated with fetal alcohol Syndrome and Down syndromeASD
Fixed splitting of S2 is heard in this condition due to excess blood in right atrium causes delay in closure of pulmonary valveASD
There is a risk of this due ASD with a DVTParadoxical Embolism
Patients with Down syndrome having a combined atrial and ventricular septal defectEndocardial Cushion Defect
The most common ASD in a patient with Down is thisOstium Primum
This condition is associated with congenital rubella and Respiratory Distress SyndromePDA
Volume overload of right heart may lead to Eisenmenger’s syndrome with reversal of shunt leading to the patient being pink in the upper extremities and cyanotic in lowerDifferential Cyanosis
Differential cyanosis is due to this ductus arteriosus connecting to the aorta after thisSubclavian Artery
Machinery murmur is heard during systole and diastolePDA
PDA can be closed with this drugIndomethacin
Intravenous indomethacin inhibits thisProstaglandin E
Complications include secondary polycythemia - due to hypoxemia causing increased EPO release, Septicemia - due to absence of filtering action of lungs, increased incidence of infective endocarditis of damaged valves, finger and toe clubbing and paradoxical embolismRight to Left Shunt
Truncus arteriosus, Transposition of great arteries, Tricuspid atresia, Tetralogy of Fallot and Total anomalous pulmonary venous return are examples of this conditionCyanotic Congenital Heart Diseases
A patient presenting with VSD, Overriding aorta, Pulmonary stenosis with RV outflow obstruction and RVHTetralogy of Fallot
The tetralogy of Fallot is the result of this during embryologyAnterosuperior Displacement of the Infundibular Septum
The most common cyanotic CHD is thisTetralogy of Fallot
The most important defect in the tetralogy of Fallot that determines the level of cyanosis effect in the newbornDegree of Infundibular Stenosis of the Pulmonary Artery
Newborn with minimal pulmonary stenosis. Acyanotic at birth since most unoxygenated blood enters lungs for oxygenationPink Tetralogy of Fallot
Newborn with severe pulmonic stenosis. Cyanotic at birth since most unoxegenated blood is shunted from right ventricle into left ventricle and out the aortaClassic Tetralogy of Fallot
Patients learn to do this to improve symptoms because of compression of femoral arteries leading to increased systemic vascular resistance leading to increased mean arterial pressure leading to decreased R -> L shunt leading to more blood directed to lung from RV for oxygenationSquatting
Squatting in the patients with tetralogy of Fallot is done to thisIncreased Systemic Vascular Resistance
X ray finding associated with tetralogy of FallotBoot Shaped Heart
A boot shaped heart seen on X-ray could be an indication of thisTetralogy of Fallot
ASD and PDA can be benefical in patient with this by increasing the oxygenationTetralogy of Fallot
Aorta arises from the RV. Pulmonary artery arises from the LVComplete Transposition of the Great Vessels
This condition is often associated with maternal diabetesComplete Transposition of the Great Vessels
Complete Transposition of the Great Vessels is associated with this condition in the motherMaternal Diabetes
Complete Transposition of the Great Vessels can be treated with this in order to keep ductus arteriosus openProstaglandin E
Pulmonary vein empties oxygenated blood into right atriumTotal Anomalous Pulmonary Venous Return
Aorta and pulmonary artery share a common trunk and intermix bloodTruncus Arteriosus
Failure of the formation of the tricuspid valve. Usually have an ASD with right to left shuntTricuspid Atresia
Characterized by segmental narrowing or constriction of aortaCoarctation of Aorta
Infantile form of the coarctation of aortaPreductal Coarctation
Adult form of the coarctation of aortaPostductal Coarctation
Constriction of aorta between the subclavian artery and ductus arteriosus. Marked decrease in blood supply to lower parts of body. Ductus arteriosus is usually patent which supplies blood to aorta distal to narrowing. Symptomatic at birth. Most infants do not survive without surgical correction. Associated with Turner’s syndromePreductal Coarctation
This condition is associatated with preductal coarctationTurner's Syndrome
Usually asymptomatic in early life. Becomes clinically evident in adolescents or adults. Constriction of aorta is distal to ligamentum arteriosumPostductal Coarctation
Clinical presentation include increased blood flow into the proximally located branch vessels, Increased BP / musculature in upper extremity, Dilatation of proximal aorta (subject to dissection), Dilatation of aortic valve ring with aortic regurgitation. Increased intracranial blood flow ; circle of Willis vessels prone to berry aneurysms and rupture. Systolic murmur between shoulder blades. Usually associated with congenital bicuspid valveProximal to Postductal Coarctation
Clinical presentation include decreased blood pressure in the lower extremity. Decreased musculature in lower extremity. Leg claudication (pain in calf or buttocks when walking) from ischemia. Decreased renal blood flow leads to hypertension due to activation of renin-angiotensin-aldosterone systemDistal to Postductal Coarctation
This develops between intercostal arteries above and below constriction. Chest radiographs shows rib notching on the undersurface of ribsCollateral Circulation in Postductal Coarctation
This condition is associated with postductal coarctation of the aortaBicuspid Aortic Valve

Pericardial Disorders

Question Answer
Pericarditis caused by viruses and bacteriaInfective Percarditis
Pericarditis direct extension of myocardial inflammation- 1-7 days post MI. Dressler’s syndrome* ( autoimmune reaction 2-8 weeks post MI)Postinfarction Pericarditis
Pericarditis caused by acute renal failureUremic pericarditis
Pericarditis caused by immune complexes usually following Rheumatic fever or SLEImmune mediated pericarditis
Pericarditis seen after Heart surgery (CABG)Postsurgical pericarditis
Paricarditis seen wit metastasis to pericardiumNeoplastic pericarditis
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Question Answer
Accumulation of exudate rich in fibrin. Often associated with pericardial effusion. Healing with fibrous tissue and calcification can cause adhesions between the pericardial layers leading to constrictive pericarditisFibrinous Pericarditis
Clinical findings include Sharp Pleuritic chest pain - Pain relieved – sitting up, leaning forward Pain increases – inspiration, leaning back Pericardial friction rub. Scratchy sound. Fever and Malaise. Diffuse ST segment elevation that is concave upwards. Pericardial effusion. If significant then can cause Cardiac tamponadeAcute Pericarditis
Compression of heart due to increase in fluid within pericardial sac. Major complication of rapidly accumulating pericardial effusionCardiac Tamponade
If slowly developing will show dyspnea and fatigueSlowly Developing Cardiac Tamponade
If rapidly developing will show cardiogenic shock. Muffled heart sound. Raised JVP. Reduced cardiac output. Pulsus paradoxus. Pulseless electrical activityRapidly Developing Cardiac Tamponade
Chronic pericarditis resulting in fibrosed, thickened, adherent and or calcified pericardium. Compresses the heart and restricts inflowConstrictive Pericarditis
The differential diagnosis of constrictive pericarditis is thisRestrictive Cardiomyopathy
Severe diastolic dysfunction. Cheat X ray: shows only mild enlargement of heart. Echo shows symmetrically thickened ventricular wall. Normal to near normal systolic function. Kussmal’s sign may be present. Apical impulse easily palpableRestrictive Cardiomyopathy
Severe diastolic dysfunction. Chest X ray: calcifications. CT: increased thickness of pericardium. Kussmal’s sign may be present. Thickness of myocardium is normalConstrictive Pericarditis
It results due to healing process after acute pericardial injury.Pericardium becomes thick, fibrous and calcified. Pericardial space obliterated and layers of pericardium fuse. Thickness of myocardium remains normalConstrictive Pericarditis