Question

Brenda, a 74-year-old woman with a history of rheumatic fever while in her twenties, presented to her physician with complaints of increasing shortness of breath ("dyspnea") upon exertion. She also noted that the typical swelling she's had in her ankles for years has started to get worse over the past two months, making it especially difficult to get her shoes on toward the end of the day. In the past week, she's had a decreased appetite, some nausea and vomiting, and tenderness in the right upper quadrant of the abdomen.On physical examination, Brenda's jugular veins were noticeably distended. Auscultation of the heart revealed a low-pitched, rumbling systolic murmur, heard best over the left upper sternal border. In addition, she had an extra, "S3" heart sound. A chest X-ray reveals a normal cardiac silhouette that is normal in diameter, but her physical examination reveals hepatomegaly and ascites, as well as pitting edema in her ankles. She is advised to wear support stockings and given a prescription for digoxin. Two weeks later she returns to the office for a follow-up visit; upon physical examination, she still has significant hepatomegaly and pitting edema, and is significantly hypertensive (i.e. she has high blood pressure). Her physician prescribes a diuretic called furosemide (or "Lasix").

1. What is the general diagnosis for Brenda’s condition? What would the diagnosis be if there were pulmonary edema instead of systemic edema?

2. Why is Brenda started on digoxin? How does it work? State your answers in terms of chronotropism and inotropism, the Na+/K+ ATPase, cytoplasmic Ca++ concentrations, and the proteins in a cardiomyocyte’s sarcomere.

3. What happened to Brenda in the two weeks before her follow-up visit? In other words, how did her body begin to compensate for decreased stroke volume? Utilize cardiac output, sympathetic nervous system, vasoconstriction to “less vital” organs (including the kidney) the renin-angiotensin-aldosterone (R-A-A) axis, Angiotensin II, ADH, pre-load and after-load, the Frank-Starling law, and the actions of digoxin.

4. Why was she given Lasix medication, and how does it work?

Answer 1

1. What is the general diagnosis for Brenda’s condition? What would the diagnosis be if there were pulmonary edema instead of systemic edema?

Edema is the condition of swelling arised due to trapping of excess fluid. Pitting edema arises due to localized vein issues or systemic problem with function of heart, kidneys, or liver function. The diagnosis of systemic edema is physical examination and its evaluation such as:

• heart failure due to jugular venous distention, crackles;
• renal disease like proteinuria, oliguria;
• hepatic diseases
• thyroid diseases.
• Constrictive pericarditis due to infection induced inflammation of the lining of heart that decreases the flexibility

2. Why is Brenda started on digoxin? How does it work? State your answers in terms of chronotropism and inotropism, the Na+/K+ ATPase, cytoplasmic Ca++ concentrations, and the proteins in a cardiomyocyte’s sarcomere.

Digoxin found to increase the heart contractility force. The machanism of action is the inhibition of ATPase that in turn control the movement of ions such as calcium, sodium, and potassium into heart muscle. It causes:

• Positive inotropism - increased contraction force.
• Negative dromotropism - decreased conduction through the atrioventricular node and
• Negative chronotropism - decreased heart rate.

3. What happened to Brenda in the two weeks before her follow-up visit? In other words, how did her body begin to compensate for decreased stroke volume? Utilize cardiac output, sympathetic nervous system, vasoconstriction to “less vital” organs (including the kidney) the renin-angiotensin-aldosterone (R-A-A) axis, Angiotensin II, ADH, pre-load and after-load, the Frank-Starling law, and the actions of digoxin.

The body compensate the fluit volume by by increasing blood pressure, holding on to salt (sodium) and water in the body, and increasing heart rate. Sympathetic nerves system stimulate hormone called norepinephrine. It also innervate hcardiac muscles which have beta-2 andregenic receptors. to which NE binds to  accelerate heart rate, widen bronchial passages, decrease motility of the large intestine, constrict blood vessels to vital organs by increasing myocardial contractility and, therefore, increase stroke volume. Renin si a proteolytic enzyme released by kidneys stimulated by the renal perfusion pressure, via stretch receptors in the vascular which inturn sense the fluid volume. Renin stimulates the formation of angiotensin which acts to stimulate thirst and increased water intake and it also stimulate ADH which constantly regulates the fluid volume in the blood. Digoxin increases the CO by improving the strength of myocardial contraction. It also works to decreases heart size, decreased venous pressure, and decreased blood volume.

4. Why was she given Lasix medication, and how does it work?

It works by minimizing the salt absorption in the body which increases the salt excretion in urine. It is used to treat edema de to congestive heart failure, liver disease, or a kidney disorder such as nephrotic syndrome.