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ENRP Exam II > Diabetes Drugs (Konorev) > Flashcards

Diabetes Drugs (Konorev) Flashcards

1
Q

Which of the following actions contributes to the anti hyperglycemic effect of insulin?

a. Activation of gluconeogenesis
b. Suppression of glycolysis
c. Activation of glycogenolysis
d. Suppression of glucose transport into cells
e. Activation of glycogen synthesis

A

e. Activation of glycogen synthesis; stimulating glucose uptake in cells (decreases blood glucose) and being stored as glycogen

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2
Q

A 24 yo woman wishes to try tight control of her diabetes to improve her long-term prognosis. Which of the following regimens is most appropriate?

a. Morning injections of mixed insulin lisper and insulin aspart
b. Injections of mixed regular insulin and upsilon glargine before going to bed
c. Morning and evening injections of regular insulin, supplemented by small amounts of NPH insulin at mealtimes
d. Morning injections of insulin glargine, supplemented by insulin lispro at mealtimes

A

d. Morning injections of insulin glargine, supplemented by insulin lispro at mealtimes

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3
Q

Hypokalemia is a side effect of insulin therapy that occurs due to:

a. increased elimination of K+ in urine
b. Increased secretion of K+ into bile
c. Increased transport of K+ from extracellular fluid into cells
d. Decreased absorption of K+ from GI tract

A

c. Increased transport of K+ from extracellular fluid into cells

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4
Q

Which of the following statements regarding Pramlintide, as an adjunct to insulin therapy, is correct?

a. Used to primarily treat T2DM patients
b. Administered orally
c. Taken before going to bed
d. Used to manage postprandial hyperglycemia
e. Known to cause hyperglycemia

A

d. Used to manage postprandial hyperglycemia

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5
Q

What are the 3 rapid acting insulins?

A

Aspart
Lispro
Glulisine

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6
Q

What is the only short acting insulin?

A

regular insulin

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7
Q

What are the 2 long acting insulins?

A

Detemir
Glargine

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8
Q

What is the one amylin analog and when is it used?

A

Pramlintide; used in combination with insulin in T1DM to enhance the effects of insulin in patients with absolute no insulin production; watch/monitor for hypoglycemia

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9
Q

What is the diagnostic criteria for diabetes mellitus?

A

increased plasma glucose levels; fasting levels over 125 mg/dl

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10
Q

How does insulin lower blood glucose levels

A

promotes intracellular glucose transport in cells via the GLUT4 transporter; activator of glycolysis and glycogen synthesis

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11
Q

When are rapid acting insulins recommended for clinical use?

A

in patients w T1DM to correct postprandial hyperglycemia; taken BEFORE the meal (sc injections only)

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12
Q

When are short acting insulins recommended for clinical use?

A

regular insulin; overnight coverage; 45 mins before meal for postprandial hyperglycemia and can be injected IV in urgent situations

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13
Q

Which insulin can be injected via IV in urgent situations of hyperglycemia?

A

regular insulin; a short acting insulin

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14
Q

What is the one intermediate- acting insulin

A

NPH; use is declining

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15
Q

When are long acting insulins recommended for clinical use?

A

basal insulin maintenance (1-2 sc injections only)

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16
Q

What is the importance of tight glycemic control in diabetic patients?

A

improves survival; reduced diabetic complications; has been shown to be effective in multiple trials

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17
Q

Why is insulin indicated to use in cases of severe HYPERkalemia?

A

insulin rapidly activates Na/K+ ATPase to shift K+ from extracellular fluid into cells

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18
Q

What is the most common and most severe adverse effect of insulin use?

A

hypoglycemia; due to delayed or missed meal, exercise, or OD of insulin

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19
Q

What is a dangerous complication in diabetic patients on a tight glycemic control?

A

hypoglycemic unawareness; they are not aware of their low blood sugar until it is dangerously low

20
Q

Amylin

A

an endogenous polypeptide synthesized by B-cells along with insulin; enhances the action of insulin

21
Q

Pramlintide

A

an amylin analog; enhances effects of insulin; used in combination with insulin in patients with absolute deficiency in insulin; watch/monitor for hypoglycemia

22
Q

Which sequence correctly describes the cellular mechanism of glucose-induced insulin release from pancreatic B cells?

a. Glucose binds to the GLUT transporter; cell membrane depolarization; increase in cellular ATP; Ca2+ channel closes
b. Glucose binds to the GLUT transporter; increase in cellular ATP; K+ channel closes; cell membranes depolarization
c. Glucose binds to the GLUT transporter; increase in glucose uptake; K+ channel opens increase in intracellular Ca2+
d. Glucose binds to the GLUT transporter; K+ channel closes; cell membrane depolarization; decrease in intracellular Ca2+
e. Glucose binds to the GLUT transporter; K+ channel closes; cell membrane hyperpolarization; increase in intracellular Ca2+

A

b. Glucose binds to the GLUT transporter; increase in cellular ATP; K+ channel closes (K+ does NOT exit); cell membranes depolarization; releases Ca2+; exocytosis of insulin release

23
Q

Which of the agents below will increase release of insulin by islet beta-cells?

a. Clonidien (alpha 2 agonist)
b. Verapamil (CCB)
c. Isoproterenol (non selective B agonist)
d. Somatostatin
e. Propranolol (non selective B blocker)

A

c. Isoproterenol (non selective B agonist); activates Gs coupled receptor; increased PKA and Ca2+ release; exocytosis of insulin

24
Q

Which of the following combinations will most likely result in developing hypoglycemia in a treated patient?

a. Glyburide + diazoxide
b. Glyburide + aspirin
c. Glyburide + a beta-blocker
d. Glyburide + a calcium channel blocker
e. Glyburide + a CYP inducer

A

b. Glyburide + aspirin

25
Q

Which of the following drugs is euglycemic?

a. Insulin
b. Glimepiride
c. Pioglitazone
d. Repaglinide
e. Tolazamide

A

c. Pioglitazone

26
Q

Which of the following drugs stimulates insulin secretion by intact pancreatic beta cells?

a. Metformin
b. Rosiglitazone
c. Pramlintide
d. Repaglinide
e. Miglitol

A

d. Repaglinide

27
Q

Endogenous factors that activate GPCR-Gs receptors on pancreatic beta cells?

A

B2-AR agonists and GLP-1 receptor agonist (incretins)

28
Q

Incretins

A

GLP-1; GI hormones that are synthesized by intestinal L-cells; promotes insulin gene expression; NOT effective as a drug due to VERY SHORT half-life (1-2 mins)

29
Q

What are two long acting GLP-1 receptor agonist?

A

Exenatide (Gila monster saliva) and Liraglutide (L=Longer half-life 11-15 hours); promotes insulin gene expression

30
Q

What are the 4 DPP-4 inhibits and what is their MOA?

A

“gliptins”
Sitagliptin, Linagliptin, Saxagliptin and Alogliptin
MOA: DPP-4 degrades GLP-1; so the inhibitor inhibits the inhibitor and increases GLP-1 which promotes insulin gene expression

31
Q

What are the K+ channel blockers

A

1st Gen: Chlorpropamide, Tolbutamide, Tolazamide
2nd Gen (higher potency): Glipizide, Glyburide, Glimepiride
Non Sulfas (Meglitinides): Nateglinide and Repaglinide

32
Q

MOA of K+ channel blockers?

A

binds SUR1-sulfonylurea receptor on the K+ channel and blocks K+ current from exiting; causes depolarization and insulin release

33
Q

Adverse effects of K+ channel blockers (Sulfonylureas)

A

hypoglycemia
weight gain (increased insulin release)
secondary failure (initially respond to tx and later build resistance)

34
Q

What drug interactions with Sulfonylureas enhance the hypoglycemic effect?

A

Salicylates/NSAIDs (aspirin), ethanol, and INHIBITING CYP enzymes

35
Q

What drug interactions with Sulfonylureas decrease their glucose-lowering effect?

A

Beta-blockers, CCBs, and INDUCING CYP enzymes

36
Q

What are the two Meglitinides that work very similar to Sulfonylureas?

A

Nateglinide and Repaglinide; K+ channel inhibition

37
Q

MOA of metformin?

A

activation of AMP-activated protein kinase; decreases gluconeogenesis; decreases glucose release; ultimately decreases insulin release

38
Q

Metformin

A

first-line treatment for T2DM; MOA activation of AMP-activated protein kinase; does NOT cause hypoglycemia or weight gain

39
Q

Adverse effects and contraindication of metformin

A

GI complications, Lactic acidosis (rare, but feared complication); contraindicated in predisposing hypoxic conditions (HF, COPD)

40
Q

What are the two Thiazolidinediones and what is their MOA?

A

“glitazones” Pioglitazone and Rosiglitazone; insulin sentinels; activates PPARy nuclear receptor; increased GLUT4 expression; onset is delayed; full effect in 1-3 months

41
Q

Which drug has been shown to delay the progression from prediabetes to T2DM?

A

the two Thiazolidinediones: “azones” Pioglitazone and Rosiglitazone; insulin sentinels; activates PPARy nuclear receptor; increased GLUT4 expression; onset is delayed; full effect in 1-3 months

42
Q

Adverse effects of the Thiazolidinediones?

A

weight gain and edema; exacerbation of heart failure (increased water retention); contraindicated in patients with CHF

43
Q

What are the 3 sodium-glucose co-tranporter 2 (SGLT2) inhibitors?

A

“gliflozin”
Canagliflozin
Dapagliflozin
Empagliflozin

44
Q

MOA of (SGLT2) inhibitors?

A

glucose is reabsorbed in the PCT by SGLT2; inhibition of this transporter increases glucose excretion and reduces hyperglycemia

45
Q

What are the 2 alpha-Glycosidase inhibitors and their MOA?

A

Acarbose and Miglitol; competitive inhibitor of alpha-Glycosidase which converts starch in the GI to monosaccharides (only form that is absorbed in the gut); decreased absorption across the intestinal epithelium; lowers postprandial hyperglycemia

ENRP Exam II (10 decks)

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