Pathology 2 - Block 1 - Part 4

davidwurbel7's version from 2016-06-03 16:55

Ischemic Heart Disease Part 1

Question Answer
Imbalance between oxygen demand and supply to the myocardium from the coronary arteries resultingIschemic Heart Disease
Reduction in coronary artery blood flow caused by obstructive atherosclerotic diseaseCoronary Artery Disease
Obstruction of a coronary artery 20% - 74%Asymptomatic
Obstruction of a coronary artery 75% - 89%Stable Angina
Obstruction of a coronary artery 90% - 95%Unstable Angina
This part of the layers of the heart gets the least amount of oxygen from coronary arteriesSubendocardium
This coronary artery supplies entire anterior portion of LV and anterior 2/3rd of IVSLeft Anterior Descending Artery
This coronary artery accounts for 40-50% of coronary artery thrombosisLeft Anterior Descending Artery
This coronary artery supplies the entire posterior and inferior part of the LV, Posterior 1/3rd of IVS, the entire RV, posteromedial papillary muscle in LV and both arterioventricular and sinoatrial nodeRight Coronary Artery
This coronary artery accounts for 30% to 40% of coronary artery thrombosisRight Coronary Artery
This coronary artery supplies the lateral wall of the LVLeft Circumflex Coronary Artery
This coronary artery accounts for 15% to 20% of coronary artery thrombosisLeft Circumflex Coronary Artery
Incidents of Ischemic Heart Disease peaks in men after this age50
Incidents of Ischemic Heart Disease peaks in women after this age70
MI restricted to only the inner 1/3 of the myocardiumSubendocardial MI
On EKG, a subendocardial MI would present as thisNon-STEMI
MI in which the entire thickness of the myocardium is affectedTransmural MI
On EKG, a transmural MI would present as thisSTEMI
This enzyme can change a stable atherosclerosis plague into an unstable atherosclerosis plagueMMPs
Is intermittent and recurrent attacks of chest pain caused by transient ( 15 sec to 15 min) reversible myocardial ischemia. Ischemia induces pain but is insufficient to cause death of myocardiumAngina
Stable angina is ischemia of this part of the myocardiumSubendocardium
Prinzmetal’s angina is ischemia of this part of the myocardiumTransmural Myocardium
Unstable angina is ischemia of this part of the myocardiumSubendocardium
On EKG, stable angina will show thisST Segment Depression
On EKG, Prinzmetal's angina will show thisST Segment Elevation
On EKG, unstable angina will show thisST Segment Depression
Angina caused by severe fixed coronary artery atherosclerosis with luminal narrowing. Predictable episodic chest pain occurs on exertion or increased demandStable Angina
With stable angina, ischemia of this part of the myocardium occursSubendocardial Myocardium
Clinical features include recurrent episodes of chest pain. Pain is substernal lasting 15 seconds to 15 minutes. Nature: Described as crushing or squeezing sometimes as burning. Radiation: to left arm or to left jaw. Associated with: diaphoresis, nausea, anxiety. Relieved by: rest (reducing the demand) or nitroglycerin or calcium channel blockers. Levine’s sign: clutching fist over sternum when describing chest painStable Angina
Uncommon form of episodic myocardial ischemia. It is caused by coronary artery spasm. Therefore, Angina occurring at rest due to coronary artery vasospasm. Patients may have significant coronary artery atherosclerosis but anginal attacks are unrelated to physical activity, heart rate or blood pressure. Ischemia not sufficient to cause necrosis of myocardial cells. Typically occurs at midnight and 8 AM, relieved by vasodilatorsPrinzmetal’s Angina
Clinical findings - ECG reveals ST elevation representing transmural ischemia. Cardiac enzymes are normal. Diagnosed by provocative testing with ergot vasoconstrictorsPrinzmetal’s Angina
This condition is treated with nitroglycerin and calcium channel blocker. Beta blockers are contraindicatedPrinzmetal’s Angina
Characterized by frequent bouts of chest pain (>20 min) at rest or with minimal exertion. Rupture of an atherosclerotic plaque with superimposed partial thrombosis and incomplete occlusion of coronary. Severe, fixed, multivessel atherosclerotic disease (> 90% blockage)Unstable Angina
A stress test for diagnosis is contraindicated if the patients has thisUnstable Angina
Stenosis of a stent is due to thisProliferation of Smooth Muscle Cells
Decreases the rate of re-stenosis in coronary arteriesStents
Stents only composed of metalBare-Metal Stents
Stents coated with anti-proliferative drugs ( paclitaxel)Drug Eluting Stents
Coronary lesions dilated with balloon inflation. Major complication is re-stenosis (15% at 6 months). Majority of patients receive intracoronary stentsBalloon Angioplasty
Used for multi-vessel coronary artery atherosclerosis. Objective is complete myocardial perfusionCoronary artery bypass graft (CABG)
Best graft patency after 10 years with this graftInternal Mammary Artery Graft
Arterialization of the vessel, fibrosis and occlusion common after 10 years with this graftSaphenous Vein Graft
Progressive congestive heart failure as a result of accumulated ischemic myocardial damage either from prior infarctions or chronic low grade ischemiaChronic Ischemic Heart Disease
Repeated minor infarcts result in replacement of cardiac tissue by non-contractile fibrous tissue. Resulting in progressive CHF due to thisSystolic Dysfunction
The most common cause of death in Chronic Ischemic Heart Disease is thisBiventricular CHF
Chronic ischemic heart disease is also called thisIschemic Cardiomyopathy
Gross and microscopic findings would show cardiomegaly due to Left ventricular hypertrophy and dilation, Fibrosis and scarring representing past healed infarcts and Coronary artery atherosclerosisChronic Ischemic Heart Disease
Unexpected death within 1 hour in a stable patient due to structural cardiac disease which may or may not have been symptomatic in the pastSudden Cardiac Death
In sudden cardiac death, death is usually due to thisVentricular Fibrillation
The most common etiology of sudden cardiac death is thisAcute Ischemia
This is triggered by acute ischemia without infarction in which positive ions flow freely into the myocardiocytes causing depolarizationLethal arrhythmias (Ventricular Arrhythmia)
Often this is the first manifestation of ischemic heart diseaseSudden Cardiac Death

Ischemic Heart Disease Part 2

Question Answer
Sudden disruption of an atheromatous plaque. Exposed subendothelial collagen or thrombogenic necrotic material. Platelet adhesion , aggregation, activation and secretion causes. Eventual formation of a platelet & fibrin thrombus. This is the pathogenesis for thisMyocardial Infarction
Platelet aggregator that contributes to formation of platelet thrombus. Vasoconstrictor that causes vasospasm of the arteryThromboxane A2


Question Answer
Cardiomyocytes do this switch to anaerobic glycolysis for ATP how long into ischemiaWithin Seconds
Cardiomyocytes lose of contractility how long into ischemiaLess than 2 min
Cardiomyocytes undergo reversible injury how long into ischemia1 - 10 min
Cardiomyocytes undergo irreversible damage and death how long into ischemia20-30 Minutes or Longer


Question Answer
The goal this is to salvage cardiac muscle at risk and to limit infarct sizeReperfusion
This can cause free oxygen radicals injury and can change the morphology of lethally injured cellsReperfusion
Reperfusion injury is due to thisFree Oxygen Radicals
Reperfusion histologically alters damaged myocardial cells producing thisContraction Band Necrosis
Seen in irreversibly damaged myocytes. Are eosinophilic transverse bands. Composed of hypercontracted sarcomeresContraction Band
Hyper-contraction of myofibrils in dead cells due to the influx of thisCalcium
Involves the full thickness of the myocardium. New Q wave develops in an EKGTransmural Infarction (STEMI)
Involves the inner third of the myocardium. Q waves are absentSubendocardial Infarction (NSTEMI)


Question Answer
Heart shows no change after an MI between the infarct and 24 hoursGross 0-24 Hours
Coagulation necrosis without neutrophil infiltrate changes in the heart after an MIMicroscopic 12-24 Hours
Heart shows pallor of infarcted myocardiumGross 1-3 Days
Myocyte nuclei and striations disappear. Infiltration by neutrophils. Neutrophils lyse dead myocardial cellsMicroscopic 1-3 Days
Macrophages begin removal of necrotic debris. Red granulation tissue surrounds area of infarction. Period of maximal softness4-7 Days
During this time period is the time most likely for ventricular rupture4-7 Days
Necrotic area is bright yellow. Granulation tissue and collagen formation are well developed7-10 Days
Infarcted tissue replaced by white, patchy, non-contractile scar tissue2 Months
MI that may occur in the elderly or in individual with DM or an individual with a high pain thresholdSilent MI


Ischemic Heart Disease Part 3
Question Answer
The most common arrhythmia after MI is thisPremature Ventricular Contraction (PVC)
The most common cause of death after MI is this arrhythmiaVentricular Fibrillation
Ventricular Fibrillation is frequently associated with thisCardiogenic Shock
MI complication that is most common on 3rd to 4th to 7th dayRupture
The most common wall rupture is thisAnterior Wall of Left Ventricular
Anterior Wall of Left Ventricular rupture will lead to thisPericardial Tamponade
Anterior Wall of Left Ventricular rupture and pericardial tamponade are usually associated with a thrombosis of this vesselLAD
MI complication with acute onset of mitral valve regurgitation and LHFPosteromedial Papillary Muscle Rupture
Posteromedial papillary muscle rupture is usually associated with a thrombosis of this vesselRCA
MI complication that produces acute VSD and left to right shunt causing RHFInterventricular Septum Rupture
Interventricular septum rupture is usually associated with a thrombosis of this vesselLAD
This complication is most often associated with LAD coronary artery thrombosis. This complication produces the danger of embolizationMural Thrombus
The combination of a local abnormality in contractility which causes stasis and endocardial damage which creates a thrombogenic surface can lead to the formation of thisMural Thrombus
Prophlylactic treatment for Mural Thrombus the long term administration of thisWarfarin and Aspirin
Warfarin and Aspirin are used for Prophlylactic treatment for Mural Thrombus because the thrombus is of this typeMixed-Type (Arterial/Venous) Thrombus
This complication is see after 1-7 days of trans-mural acute MI. It presents as substernal chest pain relieved by leaning forward, increased by leaning backwards and breathing. Pericardial friction rub is present on auscultation. Diffuse ST elevation is present is seen on EKGFibrinous Pericarditis with or without Effusion
Due to increased vessel permeability in the pericardium in which protein rich exudate form fibrous filaments produces this sound on auscultationPericardial Friction Rub
This complication develops 6 to 8 weeks after an MI. Autoantibodies are directed against pericardial antigens. Systemic S/S: Fever. Joint pain, substernal chest pain and pericardial friction rubAutoimmune Pericarditis: (Dressler’s syndrome)
This complication clinically recognized within 4 to 8 weeks. Precordial bulge during systole. Blood enters the aneurysm causing anterior chest wall movementVentricular Aneurysm
This complication presents as a double apical beat, ST segment elevation and murmur of MR (due to papillary muscle dysfunction)Ventricular Aneurysm
Complications of this complication is CHF due to lack of contractile tissue. Danger of embolization of clot material though rupture is uncommonVentricular Aneurysm
Creatine kinase and isoenzyme CK-MB, Troponin I and T, Lactate dehydrogenase and its isoenzymes and Aspartate aminotransferase (AST)Cardiac Enzymes
This enzyme appears within 4-8 hours. Peaks in 24 hours and disappears in 1.5-3 daysCreatine Kinase isoenzyme MB (CK-MB)
Reappearance of CK-MB after 3 days is suggestive of thisReinfarction.
This enzyme appears within 3-6 hours. Peak at 24 hours and disappears within 7-10 daysCardiac Troponins I (cTnI) and T (cTnT)
This enzyme is the gold standard for diagnosis of acute MI. More specific for myocardial tissue than other markers and last longerCardiac Troponins I (cTnI) and T (cTnT)
Normally this enzyme is greater in concentration than its isoenzymeLactate Dehydrogenase (LH2)
This enzyme appears within 10 hours; peaks at 2-3 days and disappears within 7 days. Mainly used to identify MI after 3 daysLactate Dehydrogenase (LH1 and LH2)
In acute MI this lactate dehydrogenase isoenzyme in cardiac muscle is released causing a flip from the normalLactate Dehydrogenase (LH1)