Explanation
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.

Explanation
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

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 skeletaland 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.

Add salmeterol to the current regimen. This patient had mild persistent asthma but was using his albuterol daily, which indicates that a step up in therapy is warranted. The preferred first line treatment regimen for moderate persistent asthma are low to medium dose inhaled corticosteroids plus a long acting beta2 agonist, as well as a short acting beta2 agonist as needed. A is incorrect. Ciclesonide is an inhaled corticosteroid. The patient in the case is already using fluticasone, so adding ciclesonide would be therapeutic duplication. C is incorrect. Long-acting beta2 agonists should only be used as adjunctive therapy in patients who are currently receiving but not adequately controlled on an inhaled corticosteroid. These medications should not be used as monotherapy, due to an increased risk of asthma related deaths. D is incorrect. Cromolyn prevents the release of vasoactive mediators from mast cell and is primarily used for exercise-induced asthma, it is not indicated as an alternative agent in patients with moderate persistent asthma. E is incorrect. Ipratropium is a short-acting anticholinergic, which is often used in COPD or in asthma exacerbations. It is not indicated for maintenance treatment of moderate persistent asthma.

Metformin is associated with vitamin B12 deficiency because it affects the calcium dependent membrane uptake of it. All other drug classes are not associated with this.