Explanation:
a. Nasal cavity: the epithelium in this zone is meant to provide a physical barrier to the invasion of microorganism or particles, it also secretes and remove mucus and foreign particles, these epithelial cells are also involved in the igE producing process (perpetuating allergic responses. <em>The nose is the first barrier to the air that enters our body, that's why the epithelial cells in this zone focus in filtering foreign particles. </em>
b. Bronchiole: epithelium is ciliated and no ciliated, it becomes cuboidal in smaller passages as it continues to branch. The no ciliated cells, also known as club cells are the ones that produce surfactant. <em>Since bronchioles are passages to direct the air to the alveoles epithelial cells in this zone have adapted to go from larger branches to smaller ones to reach the alveoli. </em>
c. Alveolus: it's composed of two types of cells, type one, that constitute the air-blood barrier and type two, cells that produce surfactant to reduce surface tension to keep the alveolus shape when breathing.<em> Since alveoli's function is to allows oxygen/carbon dioxide to move between bloodstream the epithelial cells in this organ evolved to cover this job.</em>
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Answer:
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Explanation:
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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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Answer:
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