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group_1_presentation_3_-_parkinson_s_disease [2017/12/02 12:25] tariqm2 [Epidemiology] |
group_1_presentation_3_-_parkinson_s_disease [2018/01/25 15:18] (current) |
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| ======= Coronary Heart Disease ======= | ======= Coronary Heart Disease ======= | ||
| + | {{::coronary_heart_disease_.pptx|}} | ||
| ====== Introduction ====== | ====== Introduction ====== | ||
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| {{ :screen_shot_2017-12-02_at_12.01.58_am.png |}} | {{ :screen_shot_2017-12-02_at_12.01.58_am.png |}} | ||
| - | **Figure 2:** Illustrates the observational pattern of the Electrocardiograph when the heart's electrical activity is modified. Top Left: Normal ECG Pattern, with baseline electrical levels. Top Right: Non-ST Elevation Myocardial Infarction, when there is partial blockage of the artery, the heart will show an ECG pattern with ST-depression. Bottom Right: ST-Elevation Myocardial Infarction, when there is a complete blockage of the artery, the heart will show an ECG pattern of ST-Elevation. Bottom Right: ST-Depression with T Inversion(Klabunde, 2016). | + | **Figure 2: Illustrates the observational pattern of the Electrocardiograph when the heart's electrical activity is modified. Top Left: Normal ECG Pattern, with baseline electrical levels. Top Right: Non-ST Elevation Myocardial Infarction, when there is partial blockage of the artery, the heart will show an ECG pattern with ST-depression. Bottom Right: ST-Elevation Myocardial Infarction, when there is a complete blockage of the artery, the heart will show an ECG pattern of ST-Elevation. Bottom Right: ST-Depression with T Inversion(Klabunde, 2016).** |
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| {{ ::screen_shot_2017-12-02_at_12.06.15_am.png |}} | {{ ::screen_shot_2017-12-02_at_12.06.15_am.png |}} | ||
| - | **Figure 3:** Demonstrating Cardiac Troponin-T bound to actin filaments in cardiac muscle(Melanson et al., 2007). | + | **Figure 3: Demonstrating Cardiac Troponin-T bound to actin filaments in cardiac muscle(Melanson et al., 2007).** |
| {{ ::screen_shot_2017-12-02_at_12.07.53_am.png |}} | {{ ::screen_shot_2017-12-02_at_12.07.53_am.png |}} | ||
| - | **Figure 4:** Acute myocardial infarction illustrated by soluble Troponin-T levels as high as 50 ug/L. B: Minor myocardial infarction as seen with drastically lower levels of Troponin-T in the blood, with only over 0.05 ug/L after 24-48 hours(Melanson et al., 2007). | + | **Figure 4: Acute myocardial infarction illustrated by soluble Troponin-T levels as high as 50 ug/L. B: Minor myocardial infarction as seen with drastically lower levels of Troponin-T in the blood, with only over 0.05 ug/L after 24-48 hours(Melanson et al., 2007).** |
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| {{ :diagnosis.jpg |}} | {{ :diagnosis.jpg |}} | ||
| - | **Figure 5:** Displaying cardiac catheterization beginning from a femoral artery entrance, making its way up the coronary artery to indicate the location of the plaque buildup, as well as take inter-arterial illustrations of the heart via a X-ray dye, thus conducting an angiogram(Robinson, 2011). | + | **Figure 5: Displaying cardiac catheterization beginning from a femoral artery entrance, making its way up the coronary artery to indicate the location of the plaque buildup, as well as take inter-arterial illustrations of the heart via a X-ray dye, thus conducting an angiogram(Robinson, 2011).** |
| ====== Pathophysiology ====== | ====== Pathophysiology ====== | ||
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| {{ :screen_shot_2017-11-28_at_3.21.04_am.png?300 |}} | {{ :screen_shot_2017-11-28_at_3.21.04_am.png?300 |}} | ||
| - | **Figure 6:** Demonstrates the last stage of progression of atherosclerosis in which there is thrombus formation (Radar and Daugherty, 2008). | + | **Figure 6: Demonstrates the last stage of progression of atherosclerosis in which there is thrombus formation (Radar and Daugherty, 2008).** |
| ====== Treatment ====== | ====== Treatment ====== | ||
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| {{ :screen_shot_2017-12-01_at_11.13.45_pm.png?200 |}} | {{ :screen_shot_2017-12-01_at_11.13.45_pm.png?200 |}} | ||
| - | **Figure 7:** Shows the mechanism of action of aspirin as an anti-platelet drug (Frishman et al., 2005) | + | **Figure 7: Shows the mechanism of action of aspirin as an anti-platelet drug (Frishman et al., 2005).** |
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| {{ :screen_shot_2017-11-27_at_12.06.14_am.png |}} | {{ :screen_shot_2017-11-27_at_12.06.14_am.png |}} | ||
| - | **Figure 8:** Demonstrates beta-blockers as an antagonist, and its effects by lowering heart workload in a patient with coronary heart disease (Frishman et al., 2005). | + | **Figure 8: Demonstrates beta-blockers as an antagonist, and its effects by lowering heart workload in a patient with coronary heart disease (Frishman et al., 2005).** |
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| {{ :screen_shot_2017-11-27_at_12.06.29_am.png?300 |}} | {{ :screen_shot_2017-11-27_at_12.06.29_am.png?300 |}} | ||
| - | **Figure 9:** Illustrates nitroglycerin as a precursor for nitric oxide, and its direct activation of pathways to allow vasodilation(Kukovetz et al., 1987). | + | **Figure 9: Illustrates nitroglycerin as a precursor for nitric oxide, and its direct activation of pathways to allow vasodilation(Kukovetz et al., 1987).** |
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| {{ :stents.jpeg |}} | {{ :stents.jpeg |}} | ||
| - | **Figure 10:** Illustrates a step-by-step procedure of angioplasty, which is a medicinal procedure for coronary artery disease (National Heart, Lung, and Blood Institute, 2016). | + | **Figure 10: Illustrates a step-by-step procedure of angioplasty, which is a medicinal procedure for coronary artery disease (National Heart, Lung, and Blood Institute, 2016).** |
| ====== Future Therapeutics ====== | ====== Future Therapeutics ====== | ||
