Rate of infusion: 100mL/40U × 0.03U/min × 60min/1 hr = 4.5mL/hr

Zileuton is the active ingredient found in the medicine Zyflo; a medicine that works as a 5-lipoxygenase inhibitor. As such, zileuton inhibits leukotrienes (LTB4, LTC4, LTD4, and LTE4) formation, and is used for the maintenance treatment of asthma in patients older than the age of 12. In 2 percent of patients, it raises liver enzymes. Sinusitis and nausea are the most common side effects.

Glucagon-like peptide-1 receptor agonists Sulfonylureas work in beta cells in the pancreas that are still functioning to enhance insulin secretion. Alpha-Glucosidase Inhibitors stop α-glucosidase enzymes in the small intestine and delay digestion and absorption of starch and disaccharides which lowers the levels of glucose after meals. DPP4 blocks the degradation ofGLP-1, GIP, and a variety of other peptides, including brain natriuretic peptide. Glucagon-like peptide-1 receptor agonists work in various organs of the body. Glucagon-like peptide-1 receptor agonists enhance glucose homeostasis through: (i) stimulation of insulin secretion; (ii) inhibition of glucagon secretion; (iii) direct and indirect suppression of endogenous glucose production; (iv) suppression of appetite; (v) enhanced insulin sensitivity secondary to weight loss; (vi) delayed gastric emptying, resulting in decreased postprandial hyperglycaemia. Thiazolidinediones are the only true insulin-sensitising agents, exerting their effects in skeletal and cardiac muscle, liver, and adipose tissue. It ameliorates insulin resistance, decreases visceral fat. Biguanides work in liver, muscle, adipose tissue via activation of AMP-activated protein kinase (AMPK) reduce hepatic glucose production. SGLT2 inhibitors work in the kidneys to inhibit sodium-glucose transport proteins to reabsorb glucose into the blood from muscle cells; overall this helps to improve insulin release from the beta cells of the pancreas.

A: The syndrome is an acute noninflammatory encephalopathy with hepatic failure. Although the etiology of Reye's syndrome is unknown, the condition typically follows viral illness, particularly upper respiratory tract infection (URTI), influenza, varicella, or gastroenteritis, and is associated with aspirin use during the illness. A dramatic decrease in aspirin use in children has made Reye's syndrome rare. High index of suspicion is critical for diagnosis. Consider Reye's syndrome in any child with vomiting and altered mental status. Pathogenesis is unclear, but it typically involves mitochondrial dysfunction in a viral-infected, sensitized host, usually with exposure to mitochondrial toxins (e.g., salicylates, in >80% of cases). Individuals with low levels of urea cycle enzymes are also at increased risk. Mortality has fallen from 50% to less than 20% as a result of earlier diagnosis, recognition of milder cases, and more aggressive therapy. Signs and symptoms of Reye's

syndrome include protracted vomiting, with or without significant dehydration, encephalopathy in afebrile patients with minimal or absent jaundice, and hepatomegaly in 50% of patients. Antiemetics may mask early symptoms. Liver function tests reveal elevation of ammonia levels to as much as 1.5 times normal (up to 1200g/dL) 24-48 hours after the onset of mental status changes; this is the most frequent laboratory abnormality. Transaminases (ALT and AST) increase to 3 times normal. Histologic changes include: hepatocyte cytoplasmic fatty vacuolization, astrocyte edema, loss of neurons, and edema and fatty degeneration in proximal lobules. The American Academy of Pediatrics Committee on Infectious Disease recommends that salicylate not be given to children with chicken pox or influenza B. B: Acetaminophen is incorrect. Acetaminophen acts by prostaglandin synthesis in the CNS, and this explain its antipyretic and analgesic properties, which account for its weak anti-inflammatory activity. Acetaminophen is a suitable substitute for the analgesic and antipyretic effects of aspirin in those patients with gastric complaints and to avoid Reye's syndrome in children. C: Indomethacin is incorrect. Indomethacin is more potent than aspirin as an anti-inflammatory agent (NSAID), but it is inferior to the salicylates at doses tolerated by rheumatoid arthritis patients. D: Mefenamic acid is incorrect. Mefenamic acid has no advantage over the other NSAIDS as anti- inflammatory agents. The side effects of mefenamic acid, such as diarrhea, can be severe and associated with inflammation of the bowel. E: Diclofenac is incorrect. Diclofenac is approved for long-term use in the treatment of rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis.

Correct: A. Migraine headaches typically affect females more often than males, and patients most frequently present in their early 20s. Classic symptoms of migraine include throbbing headaches lasting between 2–24 hours in duration, with triggers such as red wine, fasting, stress, and menses. Primary prevention is aimed at the identification and avoidance of triggers. Over the counter NSAIDS can be used if symptoms persist. Failing this, PRN abortive therapy is indicated, including the triptans (e.g. – sumatriptan) and metoclopramide. Choice B – Gabapentin is an anticonvulsant that is considered to be a second-line, prophylactic treatment for recurrent migraine headaches. Its utility is limited by its lengthy side effect profile. Choice C – Amitriptyline, a tricyclic antidepressant, can also be utilized for migraine prophylaxis. However, it will not abort a migraine currently in progress, and extensive side effects limit its use. Choices D + E – Propranolol and diltiazam are beta-blockers and calcium channel blockers, respectively. As with the anticonvulsants and tricyclic antidepressants, these

are considered migraine prophylaxis and will not interrupt a migraine once it has begun.

Lifelong Vitamin B12 supplementation. Vitamin B12 (cyanocobalamin) deficiency generally presents in patients as fatigue, diarrhea and headaches but can also be the cause of cognitive changes (difficulty concentrating, even mild dementia). Pernicious anemia is a macrocytic anemia, therefore laboratory findings indicate an increased mean corpuscular volume (MCV), with a decreased hemoglobin. A positive Schilling test indicates that the B12 deficiency is due to a lack of intrinsic factor. Lifelong cyanocobalamin supplementation (either orally or via injections) is needed to treat pernicious anemia. A is incorrect. Folic acid deficiency anemia is another common type of macrocytic anemia. However, cognitive deficits are not typically seen with folic acid deficiency. Furthermore, a schilling test would be negative and the methylmalonic acid (MMA) would be normal, rather than elevated. C is incorrect. Iron deficiency anemia causes a microcytic anemia, characterized by a decreased MCV. D is incorrect. A Coomb’s test is used to detect autoimmune hemolysis that may be suspected in patients with normocytic anemia (anemia with an MCV in the normal range). E is incorrect. Corticosteroids and iron supplementation are indicated as treatment in hemolytic anemia.

Use proton pump inhibitors (PPIs) in patients with or who have risk factors for osteoporosis cautiously. PPIs have been associated with a possible increased risk of bone fractures of the hip, wrist, and spine. Daily treatment with a gastric acid-suppressing medication over a long period of time may lead to hypomagnesemia. Vitamin B12 deficiency has been reported with long term use of PPIs in the literatures. The use of PPIs, may increase the risk of enteric infection by encouraging the growth of gut microflora and increasing susceptibility to organism including Clostridium Difficile. There are recent FDA warnings regarding C. Diff infection with use of PPIs. H. Pylori infection is not a complication of PPIs. PPIs in combination with certain antibiotics are used to treat H. pylori Infections.

ABW = 85 kg IBW = 50 kg + 2.3 kg (4) = 59.2 kg 85/59.2 = 1.44 AdjBW = 59.2 kg + 0.4(85 kg-59.2 kg) = 69.52

kg CrCl (IBW) = [(140-84) 59.2]/(72 × 1.4) = 32.8 CrCl (AdjBW) = [(140-84) 69.52]/(72 × 1.4) = 38.6

Pt’s weight in Kg 76.4. 76.4 × [5 mcg/kg/min] = 381.18 mcg/min Concentration of the bag [400 mg/250 mL] = 1.6 mg/ml or 1600mcg 381.18 mcg × [1 mL/1600 mcg] = 0.2382 mL/ml 60 in × [0.0.2382 mL/min] = 14.29 mL in one hour

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

This patient had hyperthyroidism, though the exact cause of her condition is not currently clear. The immediate treatment should focus on controlling the patient’s symptoms for which a non-specific beta-blocker is

seemingly an ideal choice. Propranolol therapy can be initiated without any adverse effects while the patient undergoes further workup of her condition. As the treatment for hyperthyroidism varies depending upon the cause of the condition, more definitive therapy should be avoided. Diltiazem (choice A) helps control heart rate

but does not have the same antiadrenegenic properties as beta-blockers/ The initial treatment for symptomatic hyperthyroidism is propranolol. Iodine (choice B) can be used in high doses to inhibit thyroid production of T3 and T4. Until it’s clear that this patient does not have an exogenous source of thyroid hormone (and until it is clear she is not pregnant), this agent should not be considered. Propylthiouracil (PTU) and Methimazole (choice C) inhibit the organification of iodine to tyrosine residues. If this patient has Graves diseases, this would be an appropriate treatment. Until a diagnosis is made, however, initial therapy should consist of a beta- blocker. Surgical treatment (choice E) of hyperthyroidism is often a reasonable treatment for patients who cannot tolerate medical therapy of radioactive iodine ablation.

B: Loop diuretics inhibit the Na/K/2Cl cotransporter of the luminal membrane in the ascending limb of the loop of Henle. Therefore, reabsorption of Na, K, and CL is decreased. The loop diuretics are the most efficacious of the diuretic drugs because the ascending limb accounts for the reabsorption of 25–30 % of filtered NaCl and downstream sites are not able to compensate for this increased Na load. Loop diuretics are the drugs of

choice for reducing acute pulmonary edema in congestive heart failure. Loop diuretics act promptly, even among patients who have poor function or who have not responded to thiazides or other diuretics. Adverse side effects include ototoxicity, particularly when used in conjunction with the aminoglycoside antibiotics. Furosemide and ethacrynic acid compete with uric acid for the renal and biliary secretary system, thus blocking its secretion, and thereby causing or exacerbating gouty attacks. A: Aldosterone receptor antagonist is incorrect. Spironolactone is a synthetic aldosterone antagonist that competes with aldosterone for intracellular cytoplasmic receptor sites. Because spironolactone chemically resembles some of the sex steroids, it does have minimal hormonal activity and may induce gynecomastia in males and menstrual irregularities in females. C: Inhibition of carbonic anhydrase is incorrect. Acetazolamide inhibits carbonic anhydrase, which is located intracellulary and on the apical membrane of the proximal tubular epithelium. The decreased ability to exchange NA for H in the presence of acetazolamide results in a mild diuresis. The adverse side effects of acetazolamide include metabolic acidosis (mild), potassium depletion, renal stone formation, drowsiness, and paresthesia. D: Acts as osmotic diuretic is incorrect. A number of simple, hydrophilic, chemical substances that are filtered through the glomerulus, such as mannitol and urea, result in some degree of diuresis. This is due to their ability to carry water with them into tubular fluid. Osmotic diuretics are a mainstay of treatment for patients with increased intracranial pressure or acute renal failure due to

shock, drug toxicities, or trauma. E: Blocking of the NaCl cotransporter is incorrect. The thiazide derivatives act mainly in the distal tubule to decrease the reabsorption of Na by inhibition of an Na/Cl cotransporter on the luminal membrane. As a result, these drugs increase the concentration of NA and CL in the tubular fluid. Hypokalemia is the most frequent problem encountered with the thiazide diuretics and can predispose patients on digitalis to ventricular arrhythmias. Thiazides increase serum uric acid by decreasing the amount of acid excreted by the organic acid secretory system. The thiazides inhibit the secretion of calcium, sometimes leading to elevated levels of Ca in the blood.

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

A fasting blood glucose level of greater than 7 mmol/L (or greater than 126mg/dL) is an indicator of type 2 diabetes.

0.9%= 0.9g/100mL, 120mL/h × 24hrs = 2880mL. 0.9g/100ml = x/2880ml, x = 25.92g of NaCl.

125 lb =56Kg, 56Kg × [18 units/ 1 kg] = 1022.72 units/hr, 1022.72 units × [1 mL/50 units] = 20.45 mL/hr

Agents that can cause elevated triglycerides: oral estrogens, glucocorticoids, bile acid sequestrants, protease inhibitors, retinoic acid, anabolic steroids, sirolimus, raloxifene, tamoxifen, beta blockers (not carvedilol), and thiazides.

25g/100ml = 300g/Xml Xml = 1200mL

Primary treatment for stenotrophomonas maltophilia is SMX-TMP. Meropenem, ciprofloxacin, Ampicillin and vancomycin have no coverage.

The dihydropyridine drug – nifedipine – is the active ingredient found in the medicine Adalat. Nifedipine is used to treat angina, Reynaud’s phenomenon and hypertension. It is also used as a tocolytic agent in premature labor.