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group_1_presentation_3_-_parkinson_s_disease [2017/12/02 11:16] tariqm2 |
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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| CHD incidence is on the rise worldwide and is a major cause of death in developed countries. It results in approximately one-third of deaths in individuals over the age of 35 years (Sanchis-Gomar et al., 2016). In 2016, the Heart Disease and Stroke Statistics reports that 15.5 milllion people in the USA over the age of 20 have been diagnosed with a manifestation of CHD. In the USA, approximately one-half of middle-aged men and one-third of middle-aged women develop CHD (Sanchis-Gomar et al., 2016). Despite increasing prevalence, age-standardized death rates have decreased by 22% since 1990 due to a shift in age demographics. The lifetime risk of developing CHD in individuals with more than 2 risk factors is 37.5% for men and 18.3% for women (Sanchis-Gomar et al., 2016). Estimates show that men over the age of 40 and women over the age of 45 are at most risk of CHD. Prevalence of CHD increases with age for both men and women (Sanchis-Gomar et al., 2016). | CHD incidence is on the rise worldwide and is a major cause of death in developed countries. It results in approximately one-third of deaths in individuals over the age of 35 years (Sanchis-Gomar et al., 2016). In 2016, the Heart Disease and Stroke Statistics reports that 15.5 milllion people in the USA over the age of 20 have been diagnosed with a manifestation of CHD. In the USA, approximately one-half of middle-aged men and one-third of middle-aged women develop CHD (Sanchis-Gomar et al., 2016). Despite increasing prevalence, age-standardized death rates have decreased by 22% since 1990 due to a shift in age demographics. The lifetime risk of developing CHD in individuals with more than 2 risk factors is 37.5% for men and 18.3% for women (Sanchis-Gomar et al., 2016). Estimates show that men over the age of 40 and women over the age of 45 are at most risk of CHD. Prevalence of CHD increases with age for both men and women (Sanchis-Gomar et al., 2016). | ||
| {{ :fig_11.01.jpg?nolink |}} | {{ :fig_11.01.jpg?nolink |}} | ||
| - | **Figure 1:** Outlining the Coronary Heart Disease prevalence in males and females, in differing age groups along with varying ethnicities to compare epidemiological results(Sanchis-Gomar et al., 2016). | + | **Figure 1: Outlining the Coronary Heart Disease prevalence in males and females, in differing age groups along with varying ethnicities to compare epidemiological results(Sanchis-Gomar et al., 2016).** |
| ====== Risk Factors ====== | ====== Risk Factors ====== | ||
| The exact etiology of CHD is unknown but several genetic and environmental risk factors have been associated with an increased risk of developing CHD (Torpy et al., 2009). | The exact etiology of CHD is unknown but several genetic and environmental risk factors have been associated with an increased risk of developing CHD (Torpy et al., 2009). | ||
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| Signs and symptoms for coronary heart disease (heart attack) are very similar to those who have angina, and can vary to the point where a repeated heart attack in the same patient may express different signs than the first one (NHLBI, 2015b). Also, not every heart attack begins as animated as it looks in mainstream media, with one-third of cases showing no chest pain at all (NHLBI, 2015b). Some of the most common symptoms include that of mild or severe chest pain, involving discomfort for a short (few minutes) period of time. This pain can be sharp, and feel very uncomfortable, similar to the pressure or compression felt of gastroesophageal reflux disease on the heart. There may also be some upper body discomfort, ranging from the arms to the back, shoulders, neck, jaw and/or upper pat of the stomach and below the breasts. In addition, shortness of breath can be a sign signalling discomfort to the heart, occurring either before or during the heart attack (NHLBI, 2015b). Other common symptoms include light-headedness, dizziness, nausea, vomiting, feeling unusually tired for no reason and breaking out in a cold sweat (NHLBI, 2015b). | Signs and symptoms for coronary heart disease (heart attack) are very similar to those who have angina, and can vary to the point where a repeated heart attack in the same patient may express different signs than the first one (NHLBI, 2015b). Also, not every heart attack begins as animated as it looks in mainstream media, with one-third of cases showing no chest pain at all (NHLBI, 2015b). Some of the most common symptoms include that of mild or severe chest pain, involving discomfort for a short (few minutes) period of time. This pain can be sharp, and feel very uncomfortable, similar to the pressure or compression felt of gastroesophageal reflux disease on the heart. There may also be some upper body discomfort, ranging from the arms to the back, shoulders, neck, jaw and/or upper pat of the stomach and below the breasts. In addition, shortness of breath can be a sign signalling discomfort to the heart, occurring either before or during the heart attack (NHLBI, 2015b). Other common symptoms include light-headedness, dizziness, nausea, vomiting, feeling unusually tired for no reason and breaking out in a cold sweat (NHLBI, 2015b). | ||
| ====== Diagnosis ====== | ====== Diagnosis ====== | ||
| - | |||
| - | ---- | ||
| ==== Electrocardiogram (ECG/EKG) ==== | ==== Electrocardiogram (ECG/EKG) ==== | ||
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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 ====== | ||
