N4 Pathophysiology AY 23-24

Hello, Sandylene and Group 4!

To answer your questions, 

1. Myocardial infarction (MI) causes permanent damage to the heart muscle as a result of insufficient oxygen delivery when no coronary interventions have been  performed, which is the case for our patient. MI may compromise diastolic and systolic function, which raises the risk of arrhythmia (Mechanic et al., 2023). As a result, the history of previous MI increased the patient’s risk of having another one, which also led to a further progression of atherosclerosis. The previous MI may have also led to more damage to the heart muscle, compromising the cardiac function, increasing the susceptibility to cardiac events, and in this case, another MI. Previous MI also indicates an area with permanent scar tissue which developed to repair the previously damaged heart muscles, however, compared to the original muscles this scar lacks contractility, elasticity, and conductive properties that may result in complications in pumping and blood transport. Specifically, there is cardiac fibrosis, or scarring, then stiffening of the heart which will lead to its impaired function. So, it cannot pump sufficient blood and transport as much oxygen as it could before, prior to his past MI. There was then a sudden physical exertion, when the patient was lifting heavy objects, so there was an increase in oxygen demand. But since the heart is already having a hard time pumping blood from the past MI and there is an increase in O2 demand, the heart will have to pump even harder, which in the patient’s case, is no longer possible because the heart is already impaired. The oxygen supply cannot meet the oxygen demand, thus worsening the effect of the current MI.

2. While making our diagram, we noticed that both smoking and drinking alcohol have similar mechanisms that led to the patient’s hypertension. However, there are differences in how both influenced the increase in ROS. For smoking, prolonged exposure to nicotine triggers Nicotinic Acetylcholine Receptors, whereas alcohol is metabolized by alcohol dehydrogenase (ADH) and CYP2E1 to acetaldehyde, both trigger the release of epinephrine and norepinephrine hormones.

Our group hopes that these were able to supplement your queries. Thank you so much!

Regards,

Group 3

Hello, Kateleen and Group 3!

We appreciate your questions regarding our diagram. 

To answer your questions:

1. We grouped the clinical manifestations of the patient’s ACS through discussing the complications resulting from both incidences of myocardial infarction and left-sided heart failure, as referenced by Porth’s Pathophysiology (Unit 8 - Disorders of Cardiovascular Function). From these, we traced the mechanisms leading to specific clinical manifestations exhibited by the patient.

2. Upon checking reliable resources, body fat accumulation is indeed related to dyslipidemia, wherein body fat accumulation leads to dyslipidemia. 

3. Upon counterchecking the value, we realized that it was a typo error on our end, thus we have corrected it to 92/60 mmHg. In addition, it is indeed a normal blood pressure reading, therefore, it is only a decrease in blood pressure for the patient and not a value to be categorized as hypotensive.    However, instead of categorizing it as hypotension, we decided to replace it with lowered blood pressure, as his BP reading of 92/60 is quite near the borderline for hypotension. This also indicates a concern for a sudden drop in blood pressure, as the patient is chronically hypertensive. In addition, the patient has experienced MI, which has an entailed myocardial dysfunction that can lead to hypotension.

We hope these answers have clearly addressed your questions. Thank you very much!

Regards,

Group 3

Hello, Niñaflor and Group 1! 

To answer your queries:

1. Orthopnea occurs when the person assumes supine or recumbent position because the fluid from the legs and dependent parts of the body is mobilized and redistributed to an already distended pulmonary circulation. This causes shortness of breath since this congestion causes lung stiffness and decreased lung compliance. It is relieved by standing or sitting position because gravitational forces cause the fluid to become sequestered in the lower legs and feet. Paroxysmal nocturnal dyspnea has the same mechanism with orthopnea. But it occurs after 1-2 hours of sleeping—in a supine or recumbent position. Sleeping propped up on several pillows may also provide relief.

2. As seen in the new diagram uploaded by Eron, we have taken your advice and included the mechanism as follows: Endothelial injury -> High C reactive protein (CRP) due to inflammation -> Increased uptake of LDL cholesterol by macrophages -> Foam cell formation -> Plaque formation -> Atherosclerosis.

3. While making our diagram, we noticed that both smoking and drinking alcohol have similar mechanisms that led to the patient’s hypertension. However, there are differences in how both influenced the increase in ROS. For smoking, prolonged exposure to nicotine triggers Nicotinic Acetylcholine Receptors, whereas alcohol is metabolized by alcohol dehydrogenase (ADH) and CYP2E1 to acetaldehyde, both trigger the release of epinephrine and norepinephrine hormones.

We hope these answers provided ample clarification. Thank you as well! 

Regards,

Group 3