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What Are The Side Effects Of Furosemide?
Question: Dear Doctor,
I wanted to ask if you can explain more about the mechanism action of furosemide. Thank you very much for your time.
I wanted to ask if you can explain more about the mechanism action of furosemide. Thank you very much for your time.
Brief Answer:
Questions so that I can help
Detailed Answer:
Hello,
Before I begin, I am wondering what your reason for asking this is as it is an unusual question. Sometimes we get people who are studying to be nurse practitioners, etc, asking for help on quizzes or assignments they have. I'm asking you to clarify this because if that is the case, I will write more technically with the assumption that you have some training in physiology and pharmacology. If you are writing as a patient without this background, I will try to keep it more simple and general. - Thanks
Questions so that I can help
Detailed Answer:
Hello,
Before I begin, I am wondering what your reason for asking this is as it is an unusual question. Sometimes we get people who are studying to be nurse practitioners, etc, asking for help on quizzes or assignments they have. I'm asking you to clarify this because if that is the case, I will write more technically with the assumption that you have some training in physiology and pharmacology. If you are writing as a patient without this background, I will try to keep it more simple and general. - Thanks
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Sorry i forgot to mention that part, I am asking because i am studying to be a nurse practitioner and I wanted more information on how exactly it works, and the processes. I wanted a clearer information. Thank you very much for your time
Brief Answer:
Information
Detailed Answer:
Ok, I'll try my best!
Furosemide has it's actions on the Loop of Henle by causing increased excretion of (mainly) sodium and potassium. It does this by inhibiting the Na-K-Cl cotransporter there. Because of more sodium and potassium being excreted, this creates an osmotic gradient (where there is more solute in the product/urine), and water leaves the blood and follows the higher concentration of solute, which causes an increase in water flowing out of the blood and into the urine.
Furosemide's effects on the kidneys are independent of the effects of the adrenal medullary hormone aldosterone and is also not affected by carbonic anhydrase or acidosis.
Because of the diuresis and loss of potassium as a result of the diuresis, it's important to check a patient's potassium when on furosemide or other strong loop diuretics. Furosemide decreases blood volume, and that is one of the mechanisms of it dropping patient's blood pressures (there are other mechanisms that cause this as well).
I hope this helps for what you need!
Information
Detailed Answer:
Ok, I'll try my best!
Furosemide has it's actions on the Loop of Henle by causing increased excretion of (mainly) sodium and potassium. It does this by inhibiting the Na-K-Cl cotransporter there. Because of more sodium and potassium being excreted, this creates an osmotic gradient (where there is more solute in the product/urine), and water leaves the blood and follows the higher concentration of solute, which causes an increase in water flowing out of the blood and into the urine.
Furosemide's effects on the kidneys are independent of the effects of the adrenal medullary hormone aldosterone and is also not affected by carbonic anhydrase or acidosis.
Because of the diuresis and loss of potassium as a result of the diuresis, it's important to check a patient's potassium when on furosemide or other strong loop diuretics. Furosemide decreases blood volume, and that is one of the mechanisms of it dropping patient's blood pressures (there are other mechanisms that cause this as well).
I hope this helps for what you need!
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Thank you so much doctor you explain them clearly. I think i understand more about it.
Can I please ask another question regarding another med. Sublingual glyceryl trinitrate (GTN) What i know so far that it is use to decrease the preload and afterload by relaxing and dilating the veins and arteries. Would it be possible you can also explain the mechanism of action of this drug and the process. Thank you so much for your time and hope it is not too much to ask. Thank you again.
Can I please ask another question regarding another med. Sublingual glyceryl trinitrate (GTN) What i know so far that it is use to decrease the preload and afterload by relaxing and dilating the veins and arteries. Would it be possible you can also explain the mechanism of action of this drug and the process. Thank you so much for your time and hope it is not too much to ask. Thank you again.
Brief Answer:
Information
Detailed Answer:
In the US we call it sublingual nitroglycerin. I will assume it is the same thing, but you might want to check on that as I am not familiar with GTN.
So about nitroglycerin and preload and after load:
1. Because it dilates the veins there is pooling of blood peripherally which means less blood is returned to the heart which means the left ventricle's end-diastolic pressure is reduced. That's how it decreases preload.
2. Because it causes arteriolar relaxation, there is less peripheral vascular resistance (i.e. the heart doesn't have to pump as hard to get blood to move through the arteries) and there is lower arterial pressure. This is how it decreases afterload.
Does that help make it clearer?
Are you doing a unit on cardiac related drugs? ;)
Information
Detailed Answer:
In the US we call it sublingual nitroglycerin. I will assume it is the same thing, but you might want to check on that as I am not familiar with GTN.
So about nitroglycerin and preload and after load:
1. Because it dilates the veins there is pooling of blood peripherally which means less blood is returned to the heart which means the left ventricle's end-diastolic pressure is reduced. That's how it decreases preload.
2. Because it causes arteriolar relaxation, there is less peripheral vascular resistance (i.e. the heart doesn't have to pump as hard to get blood to move through the arteries) and there is lower arterial pressure. This is how it decreases afterload.
Does that help make it clearer?
Are you doing a unit on cardiac related drugs? ;)
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear doctor,
Thank you for the response, this one still a bit unclear for me. I am studying nursing, I have to research how the drugs works and how it is used to aid people with, such as hypertension, blood pressure, increase in urine. All of this are overwhelming.
Thank you for the response, this one still a bit unclear for me. I am studying nursing, I have to research how the drugs works and how it is used to aid people with, such as hypertension, blood pressure, increase in urine. All of this are overwhelming.
Brief Answer:
Question so that I can
Detailed Answer:
It's usually more overwhelming when looking at all of it at once. Which specific thing can I help explain?
Question so that I can
Detailed Answer:
It's usually more overwhelming when looking at all of it at once. Which specific thing can I help explain?
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Yes it is, well for example if the drug was to be used for someone with an acute exacerbation of chronic left sided heart failure, how will this drug help, in terms of preload and afterload. I know it has something to do with decreasing the systolic volume in order to decrease the diastolic pressure, did i get that right.
Brief Answer:
Information
Detailed Answer:
In left sided heart failure, decreasing the left ventricle's end diastolic pressure is helpful and this is accomplished by the dilation of the venous system. Less blood volume is returned to the heart.
Decreasing the arterial resistance is helpful (decreasing the after load) because the left ventricle is stretched out in chronic left sided heart failure and does not have adequate strength of contractility. So by decreasing the resistance against which it has to pump, less contractile force is required.
Information
Detailed Answer:
In left sided heart failure, decreasing the left ventricle's end diastolic pressure is helpful and this is accomplished by the dilation of the venous system. Less blood volume is returned to the heart.
Decreasing the arterial resistance is helpful (decreasing the after load) because the left ventricle is stretched out in chronic left sided heart failure and does not have adequate strength of contractility. So by decreasing the resistance against which it has to pump, less contractile force is required.
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear Doctor, thank you so much for the response i think i understand more better now. I do have another questions about tachyapnea. How does this occur in a patient with a left sided heart failure. My answer is.... it cause by the build up of the carbon dioxide within the lungs and also cause the build up of carbon dioxide with the patient's bloodstream. I dont think its accurate. Sorry for all the questions, i hope you understand, everything is all new for me. Once again thank you for taking the time to response. It helps alot. Thank you
Brief Answer:
Information
Detailed Answer:
In heart failure, the heart is not able to pump adequately, and as there is more resistance for blood to return to the heart, fluid accumulates in the lungs (at the bases of the lungs on up) and this creates a problem with gas exchange in the lungs and so there is hypoxia too. For people with CHF, you give them supplemental oxygen to help this.
Information
Detailed Answer:
In heart failure, the heart is not able to pump adequately, and as there is more resistance for blood to return to the heart, fluid accumulates in the lungs (at the bases of the lungs on up) and this creates a problem with gas exchange in the lungs and so there is hypoxia too. For people with CHF, you give them supplemental oxygen to help this.
Note: For more detailed guidance, please consult an Internal Medicine Specialist, with your latest reports. Click here..
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
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