1What is the primary treatment for patients with Type 1 Diabetes Mellitus?
Insulin, along with diet and exercise
2What is an example of an oral antihyperglycemic medication that enhances pancreatic insulin secretion (secretagogue)?
Sulfonylureas or Meglitinides
3Which class of oral antihyperglycemic medication sensitizes peripheral tissues to insulin and is often associated with the adverse effect of lactic acidosis (rare)?
Biguanides (Metformin)
4Which group of medications impairs gastrointestinal absorption of glucose and must be taken with the first bite of a meal?
Alpha-glucosidase inhibitors
5What is the mechanism of action for SGLT-2 inhibitors?
Blocks glucose from being reabsorbed by the kidneys (proximal renal tubules), increasing glycosuria
6What type of insulin therapy includes NPH insulin, long-acting insulin analogs, or continuous delivery of rapid-acting insulin via a pump?
Basal insulin
7What is the anti-CD3 monoclonal antibody that can delay progression to symptomatic Type 1 Diabetes in presymptomatic patients?
Teplizumab
8Which injectable non-insulin antihyperglycemic medications are often used in Type 2 Diabetes treatment?
Glucagon-like peptide-1 (GLP-1) receptor agonists
9What are some common side effects of intestinal enzyme inhibitors (Alpha-glucosidase inhibitors)?
Gastrointestinal adverse effects (flatulence, diarrhea, bloating)
10Which class of non-insulin glucose-lowering drugs are also known as gliptins?
Dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitors)
11What class of antidiabetic medication does Metformin belong to?
Biguanides
12What is the primary mechanism of action of Metformin?
It primarily works by decreasing hepatic glucose production (gluconeogenesis).
13What are the most common side effects of Metformin, especially when starting treatment?
Gastrointestinal side effects, such as diarrhea, nausea/vomiting, flatulence, and abdominal pain.
14What serious but rare side effect is associated with Metformin, carrying a Boxed Warning?
Lactic acidosis
15In which patients is Metformin generally contraindicated due to an increased risk of lactic acidosis?
Patients with severe renal impairment (eGFR < 30 \text{ mL/min}), or other conditions that predispose to hypoxemia or acidosis (e.g., severe heart failure, liver impairment).
16How can patients mitigate the common gastrointestinal side effects of Metformin?
By starting at a low dose, titrating slowly, and taking the medication with food (or using an extended-release formula).
17What is a long-term nutritional side effect that can be associated with Metformin use?
Vitamin B12 deficiency
18What are key symptoms of the serious complication lactic acidosis that require immediate medical attention?
Unusual muscle pain, trouble breathing (dyspnea), extreme fatigue/weakness, stomach pain, dizziness, or feeling cold.
19Does Metformin typically cause hypoglycemia (low blood sugar) when used as monotherapy?
No, Metformin is generally associated with a low risk of hypoglycemia on its own.
20How is Metformin primarily eliminated from the body, which explains the risk in renal failure?
It is excreted unchanged by the kidneys (renal elimination).
21Symptoms of diabetic ketoacidosis
Polyuria,Polydipsia,Nausea,Fatigue,Dehydration,Kussmaul breathing,Fruity breath
22Indulin realease is decreased by
Alpha 2 agonists
23Which is an insulin analog with no peak
Glargine
24MOA of glargine
insulin binds to transmembrane receptors which activate
tyrosine kinase to phosphorylate tissue-specific substrates
25Side effect of metformin
Lactic acidosis,Gastrointestinal distress
26MOA of metformin
Increase tissue sensitivity to insulin or decrease hepatic gluconeogenesis
27MOA of acarbose
Mechanisms: inhibits α-glucosidase in brush borders of small intestine
→↓ formation of absorbable carbohydrate →↓ postprandial glucose
→↓ demand for insulin
28Side effects of suphonylureas
Hypoglycemia
– Weight gain
– Drug interactions mainly with first-generation drugs →↑ hypoglycemia with cimetidine, insulin, salicylates, sulfonamides
29MOA of sulfonylureas
Normally, K
+
efflux in pancreatic β cells maintains hyperpolarization of membranes, and insulin is released only when depolarization
occurs.
– Glucose acts as an insulinogen by increasing intracellular
ATP → closure of K
+
channels → membrane depolarization →↑
Ca
2+
influx → insulin release.
– The acute action of sulfonylureas is to block K
+
channels →
depolarization → insulin release.
30Incretin is degraded by which enzyme
Dipeptidyl peptidase 4 Enzyme
31Mechanism of action of thiazolidinediones
bind to nuclear peroxisome proliferator-activating recep
tors (PPARγ) involved in transcription of insulin-responsive genes →
-
sensitization of tissues to insulin, plus ↓ hepatic gluconeogenesis and
triglycerides and ↑ insulin receptor numbers