Scenario 1: Myocardial Infarction
CC: “I woke up this morning at 6 a.m. with numbness in my left arm and pain in my chest. It feels tight right here (mid-sternal).” “My dad had a heart attack when he was 56-years-old and I am scared because I am 56-years-old.”
HPI: Patient is a 56-year-old Caucasian male who presents to Express Hospital Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states this started this morning and has been getting worse, pointing to the mid-sternal area, “it feels like an elephant is sitting on my chest and having a hard time breathing”. He rates the pain as 9/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, or lightheadedness. Nitroglycerin 0.4 mg tablet sublingual x 1 which decreased pain to 7/10.
Lipid panel reveals Total Cholesterol 424 mg/dl, high density lipoprotein (HDL) 26 mg/dl, Low Density Lipoprotein (LDL) 166 mg/dl, Triglycerides 702 mg/dl, Very Low-Density Lipoprotein (VLDL) 64 mg/dl
His diagnosis is an acute inferior wall myocardial infarction.
Question:
Which cholesterol is considered the “good” cholesterol and what does it do?
High-Density Lipoprotein (HDL) is referred to as “good” cholesterol, as it Request Unlock removes excess cholesterol buildups in they body cells and transfers it to the liver for elimination. By doing so, it prevents cardiovascular diseases such as heart attacks and strokes, when cholesterol levels are optimal. HDL protects against atherosclerotic cardiovascular disease by preventing plaque buildup in the arteries, maintaining endothelial functions, reduces the risk of atherosclerotic cardiovascular disease, and protecting against the reverse transport of cholesterol from the tissue to the liver, where it is excreted. HDL prevents LDL from being oxidized, boosting its anti-inflammatory and anti-thrombotic effects.
Scenario 1: Myocardial Infarction
CC: “I woke up this morning at 6 a.m. with numbness in my left arm and pain in my chest. It feels tight right here (mid-sternal).” “My dad had a heart attack when he was 56-years-old and I am scared because I am 56-years-old.”
HPI: Patient is a 56-year-old Caucasian male who presents to Express Hospital Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states this started this morning and has been getting worse, pointing to the mid-sternal area, “it feels like an elephant is sitting on my chest and having a hard time breathing”. He rates the pain as 9/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, or lightheadedness. Nitroglycerin 0.4 mg tablet sublingual x 1 which decreased pain to 7/10.
Lipid panel reveals Total Cholesterol 424 mg/dl, high density lipoprotein (HDL) 26 mg/dl, Low Density Lipoprotein (LDL) 166 mg/dl, Triglycerides 702 mg/dl, Very Low-Density Lipoprotein (VLDL) 64 mg/dl
His diagnosis is an acute inferior wall myocardial infarction.
Question:
1. How does inflammation contribute to the development of atherosclerosis?
Myocardial infraction is almost often caused by Request Unlock atherosclerosis, which is an inflammatory disease. Mitochondrial damage is caused by inflammation in the heart muscle, increases free radical production, which further activates the chronic inflammatory cascade. Since plaque development erodes the artery wall, inflammation is a leading cause of aneurysms. Damage to the wounded heart may be exacerbated by an inadequate or exaggerated response to the inflammation, which causes harmful remodeling.
Scenario 2: Pleural Friction Rub
A 35-year-old female with a positive history of systemic lupus erythematosus (SLE) presents to the Emergency Room (ER) with complaints of sharp retrosternal chest pain that worsens with deep breathing or lying down. She reports a 5-day history of low-grade fever, listlessness and says she feels like she had the flu. Physical exam reveals tachycardia and a pleural friction rub. She was diagnosed with acute pericarditis.
Question:
1. Because of the result of a pleural friction rub, what does the APRN recognize?
The APRN is aware that a roughening of the usually smooth surfaces of the Request Unlock visceral and parietal pleura, as it is often seen with inflammation of the pericardium related to the pericarditis or pericardial effusion, is responsible for the pleural friction “rub” that is audible upon auscultation of the lung, towards the op of the chest and the left sternal border. Patients presenting with autoimmune illness, malignant pleural disease, pleurisy from a secondary virus or pancreatitis, or pleurisy as a result of pneumonia or a pulmonary embolisms are at a very high risk for this type of syndrome. Pleural effusion, pleuritis, and serositis are conditions that may lead to a pleural friction rub.
Scenario 4: Deep Venous Thrombosis (DVT)
A 81-year-old obese female patient who 48 hours post-op left total hip replacement. The patient has had severe nausea and vomiting and has been unable to go to physical therapy. Her mucus membranes are dry. The patient says the skin on her left leg is too tight. Exam reveals a swollen, tense, and red colored calf. The patient has a duplex ultrasound which reveals the presence of a deep venous thrombosis (DVT).
Question:
1. Given the history of the patient explain what contributed to the development of a deep venous thrombosis (DVT)
There are many contributions to the development to the deep venous thrombosis (DVT) after the surgery. First, Request Unlock venous stasis, which is caused by factors such as old age, obesity, and the inability to move around during the physical therapy. Secondly, she exhibits signs of hypercoagulability, which would indicate that her blood has an increased propensity to thrombosis, protein, and particles that may promote platelets to cling to the vessel wall and clump together, creating blood clots. Lastly, the vessel walls get damaged due to an endothelial injury, which would result in inflammation and fibrosis. The patient currently is experiencing the onset of Virchow’s triad, which includes damage and the development of a thrombosis.
Scenario 5: COPD
A 66-year-old female with a 50 pack/year history of cigarette smoking had a CT scan and was diagnosed with emphysema. He asks if this means he has chronic obstructive pulmonary disease (COPD).
Question:
1. There is a clear relationship between emphysema and COPD, explain the pathophysiology of emphysema and the relationship to COPD.
COPD is a progressive lung disease that causes lung harm due to many pathogenic mechanisms inside the Request Unlock lung. Damage to the lungs from emphysema is permanent because of the inflammatory and destructive process that occur as a result of maternal smoking or secondhand exposure. These include oxidative stress, inflammation, apoptosis, autophagy, and protease-antiprotease imbalance, which affect alveolar maintenance. Emphysema pathophysiology is characterized by substantial ventilation/perfusion mismatch due to the loss of alveoli, resulting in reduced surface area of gas exchange. The alveolar are also damaged due to the elastin breakdown inside the septa. Progressive damage from inflammatory oxidative stress is triggered by neutrophils, macrophages, and lymphocytes migrating to the lungs after prolonged exposure to the irritants. Individuals with chronic obstructive lung disease and emphysema often suffer from pulmonary infections, which are accompanied by production of large volume of sputum.