# Fitzgerald Rv test 3

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Terms in this set (86)
2 of 75A 66-year-old woman being managed for Addison's disease presents for follow-up evaluation. Findings consistent with an excessive dose of the medication taken for this condition would include:

Diffuse hyperpigmentation.
Blood pressure of 168/98 mm Hg.
Loss of axillary hair.
A white blood cell count of 6,000/mm3.
Blood pressure of 168/98 mm Hg. The first-line medication for Addison's disease is the use of a systemic corticosteroid such as oral prednisone; the goal is to replace endogenous cortisol in a manner that is consistent with the normal, physiologic diurnal variation. A typical starting dose is 15 mg q AM and 10 mg q PM. If the dose of prednisone is too high for this patient, she can demonstrate signs and symptoms of hypercortisolism, such as hypertension. Diffuse hyperpigmentation and loss of axillary hair are consistent with Addison's disease and will improve with medication. With respect to the white blood cell count, excess prednisone use will result in leukocytosis and the count will be >12,000/mm3. Topic:
A 49-year-old female of European ancestry with type 2 diabetes mellitus was started on lisinopril 20 mg tablet daily 6 weeks ago for the management of hypertension. Today her blood pressure is 128/78 mm Hg and the patient is feeling well. The appropriate action at this time would be to:

Order a white blood cell count to assess for neutropenia.
Continue on her current medication regimen.
Add oral HCTZ 12.5 mg to enhance HTN control.
Assess renal function.
Continue on her current medication regimen. Lisinopril, an angiotensin-converting enzyme inhibitor, is the appropriate class of medication in the patient with diabetes and comorbid hypertension according to the Joint National Committee 8 (JNC-8) report. Given her age and DM, her blood pressure goal is <140/90 mm Hg. She also meets the blood pressure goal per ACC/AHA guidelines that recommend <130/80 mm Hg for those with type 2 diabetes mellitus. As she is at goal, the current HTN treatment plan is adequate and can be continued. Her first-line treatment is also consistent with ADA recommendations (i.e., ACE inhibitor, ARB, calcium channel blocker, or thiazide diuretic). If in the future, HTN control is inadequate, her lisinopril dose can be increased and/or a second agent such as HCTZ can be added.
Reduces insulin resistance. Metformin has a multimodal mechanism of action that includes (1) sensitization of peripheral insulin receptors and (2) decreasing the rate of hepatic gluconeogenesis. Metformin does not facilitate renal excretion, nor does it impact the incretin system as do the DPP-4 inhibitors and GLP-1 agonists, two classes of drugs used for the treatment of T2DM.
6. When developing a management plan for a 58-year-old man with a 20-year history of type 2 diabetes mellitus, you recognize which of the following oral medications is less likely to be effective in controlling plasma glucose because of his long-standing condition?
Metformin
Canagliflozin
Glipizide
Pioglitazone
Glipizide. The pathophysiologic trajectory of type 2 diabetes mellitus is that early in the disease the beta cells of the pancreas produce supraphysiologic levels of insulin as a compensatory response to the peripheral insulin resistance and subsequent decrease in effect. However, after several years of supraphysiologic production, the beta cells eventually "burn out" and cannot produce significant amounts of insulin release. An insulin releaser, such as glipizide, will not be effective and exogenous insulin must be added to the regimen. Metformin, pioglitazone, and canagliflozin (an SGLT2 inhibitor) do not stimulate the beta cell, and their mechanisms of action are still likely to be effective.
A1c >6.5%. Diagnostic criteria for diabetes mellitus include (1) fasting plasma glucose >126 mg/dL on two occasions, (2) A1c >6.5%, (3) plasma glucose tolerance >200 mg/dL 2 hours after a 75-g glucose load, or (4) random plasma glucose >200 mg/dL along with classic symptoms of polyuria, polydipsia, or polyphagia along with unexplained weight loss or hyperglycemic crisis.
Glucose-dependent insulin release. Sitagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor. DPP-4 inhibitors slow the inactivation of two incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This ultimately increases glucose-dependent insulin release and inhibits hepatic gluconeogenesis.
9. Mrs. Griffin is a 46-year-old woman with type 2 diabetes mellitus who is using metformin and a single 10-unit daily dose of the long-acting insulin glargine. Her fasting blood glucose has been between 120-140 mg/dL (6.7-7.8 mmol/L). Which of the following best describes the next step in her therapy?
Continue on the current glargine dose
Increase her glargine dose by 2 units per day
Increase her glargine dose by 4 units per day
Increase her glargine dose by 6 units per day
The correct answer is: Increase her glargine dose by 2 units per day. The current approach to the management of type 2 diabetes mellitus is that when added, glargine insulin should begin at 10 units daily and then be titrated up or down to reach a target fasting blood glucose of approximately 100 mg/dL. When fasting blood glucose remains 141-180 mg/dL, dose should be increased by 4 units. If the fasting glucose is 120-140 mg/dL, the dose should be increased by 2 units, and when it is >180 mg/dL, the dose should be increased by 6 units. Topic: Common Endocrinopathies? Diabetes Mellitus
Correct answer is: Insulin formulation. Virtually all of the non-insulin agents used in the management of type 2 diabetes mellitus augment, either directly or indirectly, the production or action of insulin. As a result of both pharmacokinetic and pharmacodynamic properties, there is an end point that, in the best-case scenario, is approximately 2% A1c reduction. Conversely insulin, an endogenous compound, can be progressively increased in dose until the desired A1c is achieved, when other agents are noted to be effective