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Famotidine and Metoclopramide would need to be adjusted for poor renal function. Since his CrCl is less than 50, famotidine would need to be adjusted by decreasing the dose by 50% or increasing the interval to every 36 to 48 hours. Metoclopramide would also need to be adjusted by 50% of the normal dose since his CrCl is less than 40. ACEInhibitors and ARBs should be held if serum K is greater than 5.6 or there is a rise in serum creatinine greater than 30% after initiation.

Thiazolidinediones may cause fluid retention through proposed mechanism of increasing reabsorption in the collecting duct of the kidney and increasing vascular permeability in adipose tissue. Bile acid sequestrants work in the intestine to bind bile acids which doesn’t affect fluid retention. GLP-1 receptor agonists work to activate these receptors to secrete insulin from beta pancreatic cells/decrease glucagon secretion/ increase satiety and doesn’t affect fluid retention. SGLT2 inhibitors actually cause increase of fluid elimination through the kidneys. Alpha-glucosidase inhibitors work in the gut to decrease carb absorption/digestion and have no affect on fluid retention.

70% of 70 units = 49 units of Insulin Glargine daily 30% of 70 units = 21 units of Insulin Lispro daily. Dived in 3 doses would be 7 units three times a day. FT’s Insulin regimen should be 49 units of Insulin Glargine subcutaneous daily and 7 units of Insulin Lispro subcutaneous three times a day with meals

1st hour: 13mL/hr × 1 hr = 13mL 50U/mL = XU/13mL 650U Heparin given in hours since the half-life of protamine is 60 min 2nd hour 650/2 =325 units 650 units + 325 units = 975 units needs to be reversed.

**1mg of protamine reverses 100U of Heparin (1mg protamine/100U Heparin) = (x mg protamine/975U Heparin given) = x = 9.7mg protamine

Absolute risk reduction: 0.027 = 2.7% (Event rate in enoxaparin group) – (Event rate in rivaroxaban group) = (57/1473) – (17/1513) = 0.02746

Dexamethasone is used to promote fetal lung maturation. This may be necessary in cases of women who need to deliver prematurely. A tocolytic drug, such as nifedipine, may be used to suppress labor whilst dexamethasone works to accelerate fetal lung development.

Drugs mainly interact with the receptors by means of chemical forces or bonds. There are three major types of drug receptor bonds: - Covalent - Electrostatic - Hydrophobic Covalent bonds are very strong bonds and in most of the cases they are irreversible under biologic conditions. For example, the covalent bond between the acetyl group of aspirin and cyclo-oxygenase enzyme (target enzyme present on the platelets) does not breaks easily. The platelet aggregation effect of aspirin lasts long after free acetyl-salicylic acid has disappeared from the blood (about 15 minutes) and it is reversed only by the synthesis of new cyclo-oxygenase enzyme in new platelets which takes a long time. Hence the effect of aspirin is seen after the drug is stopped. Among the drug receptor interactions, electrostatic bond is much more commonly found than covalent bond. The electrostatic bonds vary from relatively strong linkages between permanently charged ionic molecules to weaker hydrogen bonds and very weak induced dipole interactions such as van der Waals force. The electrostatic bonds are weaker than covalent bonds. Hydrophobic bonds are usually very weak bonds and probably important in the interactions of highly lipid soluble drugs with the lipids of cell membranes and perhaps in the interactions of the drugs with the internal walls of receptor “pockets”.

Common GI side effects of Valproic Acid and Divalproex Sodium are Weight gain, Nausea, Vomiting, Diarrhea, abdominal pain, dyspepsia. Divalproex sodium or valproic acid affects reproductive endocrine function in women. Menstrual irregularities defined as amenorrhea, oligomenorrhea, and prolonged cycles were common. Gynecomastia is not a side effect of Divalproex Sodium. For list of drugs that causes gynecomastia refer the reference. Gingival hyperplasia is a well-known side effect of phenytoin.

LDL can be elevated by diuretics, cyclosporine, glucocorticoids, and amiodarone.

This patient shows symptoms of acute sinusitis. The most common etiology of which is viruses. Indications that an infection is viral as opposed to bacterial included a shorter infection tie (less than 10 days) and no purulent discharge (hers is watery). She does not show any evidence of a complication developing and even notes that her symptoms are improving. If her symptoms were attributed to a bacterium, then the most common cause of acute sinusitis is Streptococcus pneumoniae followed by Haemophilus influenza, then Moraxella catarrhalis. Anaerobic species such as Bacteroides fragilis and Staphylococcus aureus are more commonly found in patients with chronic sinusitis (sinusitis lasting longer than 12 weeks). This is important to realize before indiscriminately providing antibiotics for these patients.