Pathophysiology of Myocardial Infarction

Overarching Goal #6

• Myocardial infarction is caused by a blockage of a coronary artery, leading to oxygen deprivation in heart muscle cells, resulting in programmed cell death (apoptosis).
• Liporoteins are used for triglyceride and cholesterol transport. High levels of low-density lipoproteins contribute to atherosclerosis and blood clot formation.
• Macrophages ingest cholesterol, becoming foam cells. This process triggers smooth muscle cell division, leading to fatty streaks and eventual plaque formation.
• Plaque instability and rupture result in exposed collagen, triggering platelet aggregation and blood clot formation.
• A blood clot that breaks loose can travel to a coronary artery, blocking blood flow and causing heart muscle cells to become starved for oxygen and nutrients.
• Heart muscle cells cease ATP production through oxidative phosphorylation, switching to anaerobic glycolysis. This leads to lactic acid accumulation and reduced pH levels in the cells.
• Increased intracellular calcium levels and dropping pH disrupt cell-to-cell communication through gap junctions, preventing electrical signals from passing between myocardial cells.
• Cellular contents are released into the bloodstream and are detectable, indicating cardiac muscle damage.
• These processes disrupt heart rhythm and cardiac output due to the loss of functional pumping cells.
• Congestive heart failure arises when the heart cannot circulate enough blood, prompting the body to release neurohormones to maintain blood pressure, eventually leading to further damage and worsening of the heart failure condition.

Overarching Goal #5

• Blood consists of plasma (dissolved components) and cellular elements (e.g., red blood cells, white blood cells, platelets).
• Hematocrit is the percentage of red blood cells in the blood.
• Erythropoietin (EPO) is secreted by the kidneys in response to low blood oxygen levels, stimulating red blood cell production in bone marrow.
• Plasma osmolarity is regulated to maintain proper shape and function of red blood cells (RBCs) through balance of electrolytes and water.
• Hypertonic plasma causes RBCs to shrink, while hypotonic plasma causes RBCs to swell.
• Jaundice results from inefficient processing of hemoglobin metabolites in liver cells.

Overarching Goal #4

• Lymphatic fluid forms from leaked blood plasma (about 20 L daily) that reenters capillaries (17 L), leaving 3L to enter lymphatic capillaries.
• High mean arterial pressure (MAP) causes increased leakage of fluid, contributing to edema.
• Histamine causes blood vessels to dilate and become more permeable, leading to fluid leakage, edema formation, and lymphatic dysfunction.
• Problems with liver function impact protein production, influencing the balance of protein in the bloodstream and thus impacting fluid balance, which leads to fluid overload and edema.
• Obstructions in lymphatic drainage contribute to fluid buildup in tissues and edema formation.

Other Key Concepts

• Diuretics: Increase urine production, reducing blood volume and thus lowering blood pressure.
• Beta-blockers: Block beta-adrenergic receptors, slowing heart rate and reducing contractility to lower blood pressure.
• Calcium ion channel blockers: Inhibit calcium entry into cells, causing vasodilation and lowering blood pressure.
• ACE inhibitors: Inhibit the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and blood volume.
• Angiotensin II Receptor Blockers (ARBs) block the action of angiotensin II, causing vasodilation to lower blood pressure.
• COX inhibitors/Aspirin: Reduce platelet clumping, preventing clot formation.
• Tissue Plasminogen Activators (tPA) ("clot busters"): Dissolve existing clots, helping restore blood flow in blocked blood vessels.
• Inotropic agents: Drugs that increase the force of heart muscle contraction, used in heart failure.
• Hemostasis: A process that prevents blood loss by stopping bleeding.

This quiz covers the mechanisms behind myocardial infarction, focusing on the role of lipoproteins, cholesterol transport, and plaque formation in coronary arteries. Understand how these processes contribute to oxygen deprivation in heart muscle and the implications for heart health. Test your knowledge on the cellular responses involved in heart tissue damage and repair.