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.