Digoxin
Digoxin questions and answers
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Q: What would you expect if DIGOXIN after 4 years has NOT been effective?
Your 80 year old client has been on digoxin 0.25mg. p.o. once a day for four years now. What behaviours would you expect to see if his medication has NOT been effective? What things in his stimulus pool might be contributing to his increasing heart failure?
A: Are you sure its not working? Maybe if he/she wasn't on it they would have had complete heart failure several years ago. Just something to consider.
Q: Is digitek the same medication as digoxin?
I am a 21 year old heart patient who has been taking digoxin for 2 years. I recently found out about the digitek recall and want to know if I can get any compensation from the manufacture.
A: You must have damages. If you received the double strength tablets, you would have known and you would have damages. I have been a pharmacist for 30 years and this is the worst F up I have seen. Just be glad you have no damages(I hope).
Q: What effect would the acidty of orange juice have on digoxin/digitoxin over a few days?
I am a mystery writer trying to figure out if digoxin or digitoxin would be altered in a highly acidic environment like orange juice over the course of several days. I am wokring on a murder premise wherein the killer spikes orange juice with digoxin and I am wondering how long it would be potent.
A: Hi mcgo,
Check at http://www.webmd.com/. Good Luck: Blueladybug
Q: I would like to ask about taking Nitroglycrin and digoxin intake in an empty stomach?
For the people they suffer a heart failure could them to take the Nitroglycrin and digoxin as medicine for the disease while there stomachs are empty? please let me know as soon as you my good friends have the right answer.
Thank you so much for you nice sharing and help.
A: It is not necessary to take either medication on an empty stomach. Nor is it required for them to be taken with food.
Q: Does digoxin toxicity unrelated to renal failure cause hyperkalemia?
I read in this forum a related answer but ( I believe) it implies than in renal insufficiency digoxin toxicity is associated to hyper and hypokalemia, I am unable to find a reliable source. Need this to write protocols for hyperkalemia therapy
A: I believe so. The way it affects K+ (along with Na+) suggest that it is possible to have hyperkalemia unrelated to renal function. As you probably already know, Digoxin binds to a certain heart membrane pump in order to decrease functions.
I read up on the pump itself and found this: http://en.wikipedia.org/wiki/NaKATPase
I hope this sheds some light on the topic!
Q: A prescription is received in the community pharmacy for 12mcg of digoxin /lanoxin for a 6 month infant with a?
congenital heart problem to be taken once daily. The stock supply of digoxin is 0.125 mg/ 5ml. How much medication will be required for a 30 day supply of the medication ? Explain how you obtain the answer. The rest of the question is above.
A: 12mcg x 30 days = 360mcg of digoxin for the 30 days
360mcg = 0.36mg
0.36mg / 0.125mg/5mL = 14.4mL
Therefore 14.4mL of the stock supply of digoxin is required for the month supply of the prescription
Q: how does digoxin toxicity cause both hyper and hypokalemia?
Thanks a lot, it's actually for a seminar I am presenting to my pharmacy professor on digoxin toxicity.
Followup: Why do patients who are on chronic digoxin therapy present with hypokalemia when they have digoxin toxicity?
A: Digoxin is a medication utilized for the A.) treatment of supraventricular tachycardia specifically Atrial Fibrillation, and more controversially, B.) for the treatment of left ventricular insufficiency. It is a cardiac glycoside manufactured and derived from the Foxglove plant. It inhibits the Sodium-Potassium ATPase, similarly known as the Sodium-Potassium Pump. Sodium and Potassium are moved across the cell membrane via active transport. This inhibits this action, thereby inhibiting the electrical impulses in the atrioventricular node in the upper portion of the heart. In turn, the medication is utilized to control the rate in RVR (Rapid Ventricular Rate) Atrial Fibrillation, most commonly.
The hypokalemia that you see by checking electrolyte levels of the K+ (Potassium) is most frequently caused prior to the digoxin toxicity and is many times a key element to causing the digoxin toxicity. Here's what happens most often with this combination: a patient has an underlying need for K+ secondary to a reduction of intake and or excess excretion. This leads to a rapid reduction of the remainder of potassium ions available for the "pump" action we mentioned above. As a result, this is known as hypo- (lacking) kalemia (potassium). Diuretics commonly used in associated illnesses such as the first-line treatment of HTN (hypertension) & CHF (congestive heart failure), will result in increased secretion of K+ through the renal system (kidneys). This reduction of K+ from the diuretic will enhance and speed the toxic serum levels of the digitalis/digoxin.
Hyperkalemia is generally defined as the inability of the kidneys to excrete adequate levels of potassium from the body. When digoxin's mechanism kicks-in, then it decreases the use of K+ ions in the sodium-potassium pump by decreasing the NA-K ATPase activity. This reduction leads to a build-up of potassium in the body. Dehydration and various illnesses often are also contributing factors to the change to K+ levels and hyperkalemia.
Creatinine, urine K+, and Osmolarity labs would be the first step in determination of the reason for the hyperkalemia.
Treatments for digoxin toxicity includes GI decontamination and control of arrythmias & electrolyte imbalance.
I do hope this brief explanation will assist you in knowing more about the process. All my best!
For more information, talk with your local physician. They will be able to provide an up-close and personal explanation inclusive of some drawings and texts that you can read. Also, Wikipedia is usually a fair source of basic to moderate level information on a subject. You might want to search these key words: hypokalemia, hyperkalemia, digoxin toxicity, ATPase, and cardiac glucosides. These will lead you to a better definition of the keywords in my response. Good luck!
Sincerely,
Nathaniel - Paramedic
Q: My mother was a victim of Digoxin poisoning. Can I file for her and include my sister in the lawsuit as well?
I would like to file a lawsuit for my mother who suffered from the drug Digoxin. Can I include my sister in the case as well. She is as concerned by my mom as I am. My mother is still taking this drug due to her doctor prescribing it to her. I have seen where this item should have been taken off of the market.
A: i'd say do more research. You won't get many answers on here. Any good ones at least.
Q: Why do patients who are on chronic digoxin therapy present with hypokalemia when they have digoxin toxicity?
I'm a pharmacy student so you can use medical jargon on me.
A: Digoxin toxicity can occur with any condition that increases total body levels of Digoxin or modifies the cardiac sensitivity to Digoxin. Digoxin toxicity can occur with hyperkalemia, hypokalemia or normokalemia. Hypokalemia potentiates the toxicity from Digoxin and Digoxin toxicity can occur with lower serum concentrations of Digoxin in the presence of hypokalemia. Severe acute Digoxin toxicity will frequently produce a hyperkalemia.
Digoxin inhibits the Sodium/Potassium ATPase, which leads to increased intracellular Sodium concentrations. This results in a decreased transmembrane Sodium gradient, which is the driving force for the Sodium/Calcium transport. This results in increased concentration of Calcium in the cell, which increases the strength of cardiac contractions. Potassium competes with Digoxin for the alpha subunit of the Na-K-ATPase enzyme. Hypokalemia results in less potassium available to compete with Digoxin, which results in more Digoxin binding to the enzyme therefore more toxicity. Hypokalemia decreases Na-K-ATPase activity, thereby exacerbating the principal cellular derangement of cardiac glycoside toxicity. Acute severe Digoxin toxicity usually produces hyperkalemia, because of the inhibition of Na-K ATPase pump resulting in increased extracellular potassium. The severity of acute Digoxin toxicity is positively correlated with the degree of hyperkalemia. I hope I answered your question, but if not let me know. It can be confusing. Good luck with your school.
Q: What would happen if a patient was given a double dose of digoxin for two weeks.?
I am a pharmacy intern and my pharmacy manager asked me this question and I can't find what would happen. Please include where you got your sources. Thanks!
A: The correct answer is "It depends." It depends on the following things: Digoxin level, renal function, comorbidities, other medications they are taking (i.e. amiodarone, quinidine, verapamil), electrolytes (esp. hypokalemia and hypomagnesemia) etc... If the digoxin level comes back toxic (usually > 2.5), the patient may experience signs / symptoms of dig toxicity. Early symptoms include nausea & vomiting, loss of appetite, diarrhea, headache, and weakness. Later symptoms may include visual disturbances (the classic halo effect that you always here about), confusion, seizures, cardiac dysrhythmias, hallucinations, and even death. Every patient is different and will respond differently. If the patient is in dig tox, you give Digibind. Hope this helps.
Q: What is the toxicity of digoxin?
Can it really bring the heartbeat to a dead stop? Is this true, literally? Is it just one extra dose or is it like a dozen or more overdoses which can do this? How narrow is the margin?
A: Digoxin's narrow therapeutic range (0.8 to 2 ng/ml) makes toxicity quite common: It's estimated to be present in 5% to 20% of all hospitalized patients on digoxin. Testing serum drug levels about 8 hours after each drug administration helps detect toxicity. Log and report digoxin levels greater than 2 ng/ml and a heart rate below 60 bpm; these are key indicators of digoxin toxicity, though many patients who are on digoxin routinely have heart rates below 60 bpm.
Renal insufficiency, drug interaction, hypercalcemia, hypokalemia, hypomagnesemia, hypothyroidism, and advanced age all increase the risk of digoxin toxicity. (See Raising the Risks for common drugs that can cause problems.) Gastrointestinal symptoms of toxicity include anorexia, nausea, and vomiting. Neurologic symptoms include headaches, malaise, fatigue, neuralgic pain, dementia, seeing yellow or green halos around objects, and seizures. Cardiac signs include functional rhythms, heart blocks, ventricular rhythms, acute tachycardia, and bradycardia.
Q: how much of Ouabain gives the same inotropic effect of Digoxin?
Ouabain is the cardiac glycoside that is widely used in research while Digoxin is the most clinically used as an inotropic agent.The question is how much Ouabain is equivalent to Digoxin ? please guide me to the source of information.
A: I am a pharmacist and I am not aware of the existence of equivalency data. You would be safer to use Digoxin exclusively, it's dosage and monitoring parameters are well known.
Q: Where would Digoxin go on the Schedules of Controlled Substances?
A: Digoxin is a prescription-only medication, but not a controlled substance.
Usually, the schedule of a drug really only matters if it is a controlled substance (schedule 1-5). These are ranked more or less by how likely they are to be abused or cause addiction.
Sometimes drugs like digoxin (prescription but not controlled) are classified as schedule 6, but usually, when something is said to be "scheduled", it means schedules 1-5.
Hope that helps!
Q: I want to know what is in the drug that the FDA recalled it is called DIGITEC or digoxin?
I told you all I know. The FDA recalled digixon and I took it this morning!
A: Note: It is NOT ALL digoxin - just the ones from this one manufacturer. The rest are fine. Your prescription label should say who manufactured the tablets you have.
Q: What is the maximum dose of oral Digoxin for a 4- month old baby!?
The baby is 4 months old and weighing 7 Kg. Could the maximum dose be 250 microgram per day per oral??
A: The maximum daily dose would be 84mcg/day. This is based on a dose of 12mcg/kg/day. Consult a Physician for the appropriate dose.