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Nr 565 Advanced Pharmacology Final Exam Online Study Guide | Professor Verified | Latest Edition (Just Released)

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NR 565 ADVANCED PHARMACOLOGY FINAL EXAM ONLINE STUDY GUIDE | PROFESSOR VERIFIED | LATEST EDITION (JUST RELEASED)

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NR565 Advanced Pharm: Final Study Guide

1. Glycemic Goals in - A1c: <7.0%
Diabetes - Premeal plasma glucose: 70-130 mg/dL
- Peak post-meal plasma glucose: <180 mg/dL

2. Diabetic Diabetic nephropathy is a serious complication of diabetes characterized by kid-
Nephropathy ney damage. Preventive strategies include:
Prevention - Blood Sugar Control: Maintaining tight glycemic control through lifestyle
changes and medication (e.g., metformin, insulin) can slow the progression of
kidney damage.
- Blood Pressure Management: Keeping blood pressure within target ranges
(usually <130/80 mm Hg) using ACE inhibitors or ARBs can protect kidney func-
tion.
- Regular Monitoring: Routine screening for albuminuria (protein in urine) and
kidney function helps detect early changes.
- Lifestyle Modifications: A balanced diet low in sodium and protein, regular
physical activity, and weight management are critical.
- Avoiding Nephrotoxins: Limiting the use of medications that can harm the
kidneys (e.g., NSAIDs) and avoiding excessive alcohol and smoking.
- Patient Education: Teaching patients about diabetes management and the
importance of regular check-ups.

3. 1st Generation vs - Both generations reduce glucose levels to the same extent.
2nd Generation - How do the generations differ? The second-generation agents are much more
Sulfonylureas potent than the first-generation agents, and hence dosages are much lower (as
much as 1000 times lower in some cases).
- With second-generation agents, significant drug-drug interactions are less
common, and the outcomes tend to be milder. Because of these differences, the
second-generation agents have nearly completely replaced the first-generation
agents in clinical practice.

4. Dipeptidyl Pepti- Generally well tolerated: Rarely, patients have developed pancreatitis, including
dase-4 Inhibitors fatal hemorrhagic or necrotizing pancreatitis according to post-marketing reports.


, NR565 Advanced Pharm: Final Study Guide

(DPP4I): Adverse
Effects

5. Dipeptidyl Pepti- - Enhances the actions of incretin hormones, endogenous compounds that (1)
dase-4 Inhibitors stimulate the glucose-dependent release of insulin and (2) suppress the post-
(DPP4I): MOA prandial release of glucagon (a hormone that increases glucose production in
the liver).
- Both actions help keep blood glucose from climbing too high. How does
sitagliptin boost incretin actions? It inhibits DPP-4, an enzyme that inactivates the
incretin hormones.

6. GLP-1 Receptor Activates receptors for GLP-1- slowing gastric emptying, inhibits glucagon, sup-
Agonists: MOA presses appetite, and stimulates glucose-dependent release of insulin.

7. GLP-1 Receptor Patients should monitor blood glucose regularly.
Agonists: Moni-
toring

8. Incretin Mimetics Injectable medications that mimic the action of incretin hormones (like GLP-1) to
enhance insulin secretion, suppress glucagon release, slow gastric emptying, and
promote satiety, thereby helping to control blood glucose levels in patients with
type 2 diabetes.

9. Incretin Mimetics Incretin mimetics are generally not recommended during pregnancy due to
in Pregnancy insufficient safety data. Managing diabetes in pregnant women typically focuses
on insulin therapy and dietary modifications.

10. Meglitinides vs - Meglitinides (e.g., repaglinide) stimulate insulin secretion from the pancreas
Sulfonylureas but have a shorter duration of action, making them suitable for controlling post-
prandial glucose levels.
- Sulfonylureas (e.g., glipizide) also stimulate insulin release but have a longer
action. Both classes can cause hypoglycemia, but meglitinides may have a lower
risk.


, NR565 Advanced Pharm: Final Study Guide

11. Metformin: MOA Lowers blood glucose and improves glucose tolerance in three ways:
- inhibits glucose production in the liver
- reduces (slightly) glucose absorption in the gut
- sensitizes insulin receptors in target tissues (fat and skeletal muscle) and thereby
increases glucose uptake in response to whatever insulin may be available. In
contrast to sulfonylureas, metformin does not stimulate insulin release from the
pancreas. As a result, metformin does not actively drive blood glucose levels down
and hence poses little if any added risk for hypoglycemia when used alone.

12. Metformin: Preg- - Metformin has been used during pregnancy. However, insulin is preferred as it
nancy does not cross the placenta or enter breast milk in significant amounts.
- Most oral diabetes medications are generally avoided during pregnancy and
breastfeeding.

13. Metformin: Side - GI disturbances: nausea, diarrhea, and decreased appetite.
Effects - Altered nutrient absorption of vitamin D and folic acid, potentially leading to
pernicious anemia.
- Metabolic acidosis: black box warning of this severe side effect, with clients with
renal impairment particularly at risk.

14. Pioglitazone - Weight gain, edema, and an increased risk of heart failure and bone fractures.
(TZD): Adverse - Long-term use may be associated with an increased risk of bladder cancer.
Effects

15. Pioglitazone A thiazolidinedione (TZD) that works by activating PPAR-γ receptors, leading to
(TZD): MOA increased insulin sensitivity in peripheral tissues and improved glucose uptake.

16. Repaglinide - Patients should be educated on taking repaglinide before meals to effectively
(Meglitinide): manage postprandial glucose levels.
Patient - They should also be informed about the risk of hypoglycemia and the importance
Education of monitoring blood glucose.

17.

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