There are fewer antifungal, anti protozoan, and antihelminthic drugs compared to antibacterial drugs because these cells can be similar to human cells and therefore they can not achieve selective toxicity.
<h3>What is drug selective toxicity?</h3>
The expression 'drug selective toxicity' makes reference to the ability of a specific medication to discriminate between cells of different organisms (in this case human cells and other types of eukaryotic cells).
Drug selective toxicity is a fundamental issue during drug discovery and drug development.
In conclusion, there are fewer antifungal, anti protozoan, and antihelminthic drugs compared to antibacterial drugs because these cells can be similar to human cells and therefore they can not achieve selective toxicity.
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Answer:
Hepatocytes secrete Bile
Explanation:
Hepatocytes are the epithelial cells of the main parenchymal tissue. The hepatocytes are present in the liver. 70-85% of the liver consists of the hepatocyte cells. The hepatocytes are responsible for the synthesis and secretion of the bile into a system of tiny bile canaliculi, present between hepatocyte cells.
Answer: d. autonomic nervous system
Explanation:
The dilation of the pupil occurs due to the radial muscles. This is controlled by the autonomic nervous system. The autonomic nervous system consists of sympathetic and parasympathetic nervous system. The sympathetic nervous system controls the dilation of pupil whereas the parasympathetic nervous system controls the contraction of pupil.
A dilation response generally involves the widening of the pupil that may be caused by the adrenaline and drugs like cocaine, MDMA, amphetamines, hallucinogens and dissociatives.
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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