Answer:
yes that's correct but what are we answering then?
Explanation:
A typical neuron consists of a cell body (soma), dendrites, and a single axon. The soma is usually compact. The axon and dendrites are filaments that extrude from it. Dendrites typically branch profusely and extend a few hundred micrometers from the soma. I know that this only answers part of it, but I hope this helps.
Answer:
3 Monitor intake and output
Explanation:
This client is admitted for heart failure and acute pulmonary edema, which means that his/her heart is not pumping blood as it should, and that there's liquid in the lungs, causing the client symptoms such as dyspnea (shortness of breath).
IV Furosemide, a loop diuretic is prescribed. This drug increases renal excretion of water and electrolytes out of the body, resulting in the mobilization of excess fluid from the body and a decrease in blood pressure. The indication to give the client a second dose of furosemide in an hour is because of its delayed effect.
Since furosemide causes liquids to exit the body, it is important to monitor fluid balance in order to evaluate the effectiveness of this medication. Monitoring fluid balance refers to observing and registering all liquids that come in (IV, orally) and out (urine) of the body. For the client, being admitted to the hospital and receiving IV medication, the nursing personnel should be registering all the liquids the client is receiving (IV and orally) and voiding (urine).
Subsequent INR readings are influenced by the dose, method, and initial INR of vitamin K. For intravenous vitamin K doses of 2 mg or more, INR decrease is comparable. FFP preadministration has no effect on INR readings 48 hours or more after vitamin K administration.
What is Abstract of Vitamin K dosing to reverse warfarin based on INR, route of administration, and home warfarin dose in the acute/critical care setting?
- Commonly, vitamin K is used to reverse the anticoagulant effects of warfarin. The ideal vitamin K dosage and delivery method that does not lengthen bridging therapy are still unclear.
- To ascertain the elements affecting the level and pace of vitamin K-induced INR reversal in the acute/critical care setting.
- 400 patients' charts from between February 2008 and November 2010 who got vitamin K to counteract the effects of warfarin were examined. International normalized ratios (INRs), intravenous or oral vitamin K doses, and whether or not fresh frozen plasma (FFP) was administered were among the information gathered. INRs were measured 12, 24, and 48 hours before vitamin K treatment.
- At baseline, 12 hours, 24 hours, and 48 hours, respectively, intravenous vitamin K decreased INR more quickly than oral vitamin K (5.09, 1.91, 1.54, and 1.41 vs. 5.67, 2.90, 2.14, and 1.58). Subsequent INR values were impacted by baseline INR (p 0.001), method of administration (p 0.001), and vitamin K dosage (p 0.001). For intravenous vitamin K doses of 2 mg or more, there was a similar drop in INR. Home warfarin dose had no effect on INR responses to intravenous or oral vitamin K (p = 0.98 and 0.27, respectively). FFP had no effect on INR readings 48 hours later. Although larger vitamin K doses and longer anticoagulation bridge therapy appeared to be related, neither the incidence (p = 0.63) nor the duration (p = 0.61) were statistically significant.
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