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62 Cards in this Set
- Front
- Back
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What are the 4 types of ischemic heart disease? Which of these diseases are considered to be acute coronary syndromes?
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-Angina pectoris (stable, unstable)
-Sudden cardiac death -Myocardial Infarction -Chronic Ischemic Heart disease Acute syndromes: unstable angina, sudden cardiac death, and mycardial infarction |
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What is angina pectoris? When would a pt. typically feel angina pectoris?
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A transient reduction in flow or supply/demand mismatch. No myocyte necrosis
Angina pectoris is typically felt during exertion and alleviated with rest |
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Pt. presents with transient, radiating retrosternal pain that increases with exertion.
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Angina pectoris
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What is Prinzmetal's angina?
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Angina that may occur during rest (which typically does NOT happen) from vasospasms (NOT ischemia)
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What is unstable angina?
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Angina that is occurring more frequently and there is merging of attacks (attacks can even be at rest).
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What is the pathology occurring during unstable angina?
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There is a thrombi overlying a atherosclerotic plaque, but it quickly lyses and flow is quickly restored
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What are most cases of angina pectoris related to?
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-Coronary atherosclerosis, valvular dysfunction, and dysrythmias (less often)
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How can dysrrythmias cause an episode of pectoris angina?
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The increase in ventricular contractions during a dysrythmia can prevent the proper filling of the ventricle, and as a result there is decreased coronary flow (decreased O2 supply)
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This type of ischemic heart disease can be fatal within 24 hours of onset.
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Sudden cardiac death
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What causes sudden cardiac death?
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-related to dysrrythmias
-may occur during a MI -May occur in the absence of clinical history of ischemic heart disease |
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What are 2 good explanations for why we consider sudden cardiac death an abrupt event?
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1. occurs immediately or within 24 hours
2. Appears acutely; can happen with or without a prior history of ischemic heart disease |
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What is the major difference between the pathology of angina pectoris and MI?
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Angina pectoris is TRANSIENT and doesn't have myocyte necrosis
MI's involve myocyte necrosis |
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This type of ischemic heart disease is related to arterial spasms.
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Prinzmetal's (stable) angina
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What is the pathology behind an MI?
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Sudden decrease or occlusion of coronary flow to myocytes or mismatch of myocardial oxygen demands that leads to myocyte necrosis.
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What is the window of opportunity to prevent myocyte necrosis?
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If the person receives medical attention within 20 mins of onset. Beyond that, there will be myocyte necrosis (20-40 mins)
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What is the pathology behind chronic ischemic heart disease?
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Coronary insuffiency to the myocardium which leads to multiple, tiny ischemic events; may precede or follow a MI
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What condition can develop from chronic ischemic heart disease?
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CHF
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The major reason for decreased coronary flow in ischemic heart disease is due to?
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Coronary atherosclerosis
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What is the peak age of incidence of an MI in men and women?
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Men: 55-64
Women: 70-80 Men are more likely to experience an MI before women, BUT the risk for women increases with age. More of a 1:1 ratio for older women and men. |
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Although there are many exceptions, how many coronary arteries are involved in atherosclerotic occlusion? What percentage of narrowing increases the risk of an ischemic event?
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Usually involving more than 1 coronary artery
-75% blockage increases risk |
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Explain the events that follow the rupture of a atherosclerotic plaque? Where does this rupture typically happen?
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-The rupture of the plaque typically occurs at the shoulder
-This rupture can cause thrombus formation which will further occlude the artery & possibly lead to an embolus. |
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What are the precipitating factors that can occur within the vessel wall & lead to an MI?
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-rupture of the plaque --> leads to thrombi formation
-bleeding into the plaque --> increases the size of the plaque -coronary vasospasm causing further decrease in coronary flow -increased O2 demand for myocardium -Hypotension (due to decreased coronary flow) -Tachycardia and valve dysfunction |
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Where is inflammation typically seen in an athersclerotic plaque?
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The shoulder of the plaque
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Unstable angina, cardiac sudden death, and MI are examples of ____________?
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Acute coronary syndromes
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What is occuring during an acute coronary syndrome?
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There is an acute change in the in the athersclerotic plaque.
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What factors can cause disruption of a plaque?
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-Vasospasm
-tachycardia -changes in pressure and flow through coronary a. -inflamation |
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Explain the role of inflammation in a plaque? What can occur as a result of inflammatory cells in an atherosclerotic plaque?
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-The inflammatory cells (found in the shoulder of the plaque) can release mediators, including ezymes that break down the plaque & cause disruption
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In this type of ischemic heart disease, there is plaque disruption and thrombi formation, but the thrombi quickly lyses.
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Unstable angina
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What are the various things that a thrombi can do once formed in a vessel?
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1. Can lyse quickly after its formation (unstable angina)
2. Occlude the vessel and decrease flow, leading to necrosis 3. The thrombis can break up into smaller thrombi and move into other arteries 4. Thrombi can organize itself: growth of endothelial cells into it and it moves to become incorporated into the plaque which increases the size of the plaque. |
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What is meant by thrombus organization?
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Incorporation of a thrombi into a plaque which increases the size of the plaque.
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There are 2 types of MI's. What are they, and how are they different?
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There are transmural & subendocardial MI's
Transmural infarctions: involves the entire thickness of the ventricular wall. Subendocardial: involves the inner third/half of the ventricular wall. |
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In a transmural myocardial infarction, the best way to determine the vessel that has been occluded is to __________?
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Identify the area of the myocardium that has been affected
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What area of the myocardium is most vulnerable to coronary ischemia? Why?
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The subendocardium: because when the coronary vessels dip into the myocardium the subendocardium is the last region of perfusion, and also...
The subendocardium is an area that's HIGHLY contracted during systole and therefore the vessels in this area can be contracted |
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What is an aborted transmural infarct? What area is damaged in this event? Why?
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This is when an occlusion has occurred, however that area of the heart is reperfused before the ENTIRE wall is affected (defined by a single vessel occlusion)
The area that is affected is usually limited to the subendocardium since they are the last area of the myocardium to be perfused |
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Explain the areas of the heart that would be affected first and last in an MI?
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A transmural infarct occurs in waves; so the area that will be affected first is the last area to receive blood supply (the subendocardium) and if necrosis continues, then the myocardium. If perfusion happens quickly enough, then the myocadium will be preserved and the only area affected will be the subendocardium.
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What is the difference between the necrosis pattern in a transmural vs. subendocardial MI?
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Transmural infarctions are those that involve necrosis due to the occlusion of ONE vessel, so you are able to identify vessel involved by the area of necrosis
Sudendocardial infarctions are DIFFUSE reductions in flow/ increased demand (unless its an aborted transmural infarct). These infarctions only involve the inner 1/3 - 1/2 of the wall |
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A subendocardial infarct is likely to happen in a person who is __________? Why?
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Hypotensive; because SE infarcts show a pattern of DIFFUSE reduction in perfusion.
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As an occlusion occurs, there are changes within the heart tissue. What are these changes and in what order do they occur?
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Myocardial function becomes abnormal --> subcellular changes (organelles) --> histological changes --> gross pathological changes
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Describe the histological features seen in myocardium after 1 to 2 hours? Why does this happen?
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The myocardium has a change in contractility because the myofibers take a wavy appearance because of the viable myocardium pulling on the areas of necrotic myocardium
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Describe the condition of the myocardium 4-12 hours after an MI.
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-early coagulation necrosis
-influx of neutrophils -interstitial edema & hemorrhage |
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What is the most prominent histological feature seen 4-12 hrs. after an MI?
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coagulation necrosis = no visible nuclei present in the myocardial cells & loss of cross striations
Also, neutrophil influx and extravasated RBC's |
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18-24 hours into an MI, what will you see histologically?
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More coagulation necrosis and more neutrophils
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What is the state of the myocardium 24-72 hours after an MI?
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Total necrosis & peak neutrophil infiltration and necrotic debris
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What process occurs at the end of the first week of an MI? What does this process entail?
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Repairative changes begin to occur. Clearing of dead cells
Early granulation tissue replaces myocardium |
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What does granulation tissue consist of?
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matrix + capillary tissue (weak soft tissue)
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Once myocardium has been damaged, can it be regenerated?
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No, it is replaced with granulation tissue
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Eventually, granulation tissue is replaced by ________? When does this occur?
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Fibrous tissue (3-4 weeks later)
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Gross changes to the heart will only be seen after _____________ hours.
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18-24 hours
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Describe the evolution of GROSS changes that occurs after an MI?
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The changes begin 18-24 hrs. later when areas of pallor or hyperemia.
24-72 Pallor with hyperemic border 3-7 days Granulation tissue present 10 days: depressed, soft, gelatinous appearance Weeks-months: Pale, gray fibrotic scar |
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Which day of evolution is the heart particularly vulnerable? Why?
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At days 3-7 because the granulation tissue is very soft and the ventricular wall is vulnerable to rupture due to the softness.
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What are the common complications of an MI?
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-Dysrhythmia (75-95%) - may be transient of long standing
-CHF -Cardiogenic shock Recurrent infarction (of the same or different area) |
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On days 3-7 a pt. is most vulnerable to _________?
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Ventricular rupture with hemopericardium and tamponade
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How can the papillary muscles be affected after an MI? What can this lead to?
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They can rupture, leading to the acute onset of mitral valve insufficiency
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As the myocardium is healing, what is the patient at risk for?
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The development of a thrombus overlying the infarct and the danger of it embolizing to systemic circulation
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What is a patient at risk for if the infarcted area were to expand?
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Ventricular aneurysm - the zone of myocardium is stretched out bc viable myocardium is pulling on the necrotic myocardium.
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Describe the ventricular wall after a ventricular aneurysm.
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The ventricular wall is thinned out with the presence of fibrous tissue.
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What problems are associated with ventricular aneurysm?
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-the increased risk of thrombus formation due to change in blood flow
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Describe the appearance of myocardial tissue in the following states:
-less than 20 mins -2-4 hours after the MI -permanent occlusion |
-tissue is salvagable
-partial salvage -complete infarct |
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Why can there still be some subcellular damage to the myocardium despite repurfusion?
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-Due to free radical formation, neutrophils,and abn. Ca transport across the membrane so there is still potential for damage.
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How does chronic ischemic heart disease occur?
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After multiple previous episodes of ischemic events
-may or may not follow angina or an MI -Highly related to coronary atherosclerosis |
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What are the histoloigcal indicators of chronic ischemic heart disease?
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Patchy fibrous scars with diffuse interstitial fibrosis
-hypertrophy of myocytes adjacent to scars |
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What histological process can occur in association with chronic ischemic heart disease? What does this pathological process involve? Where does this process typically take place
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Vacuolar degeneratation of myocytes
-sublethal ischemic change (potentially reversible) -seen at the edges of an infart (MI) or chronic ischemic heart disease |
