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Endo Repro Exam II > Drugs used in Diabetes > Flashcards

Drugs used in Diabetes Flashcards

1
Q

Rapid, short, intermediate, and long-acting insulins used in tx of diabetes

A

Rapid acting: Aspart, Lispro, Glulisine

Short-acting: regular insulin

Intermediate acting: Neutral protamine hagerdorn (NPH)

Long-acting: detemir, glargine

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2
Q

Amylin analog used in tx of diabetes

A

Pramlintide

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3
Q

Of the insulin secretagogues used to treat diabetes, there are incretin mimetics and K(ATP) blockers. Of the Incretin mimetics, what drugs fall into the GLP-1 agonist category?

A

Exanatide

Liraglutide

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4
Q

Of the insulin secretagogues used to treat diabetes, there are incretin mimetics and K(ATP) blockers. Of the Incretin mimetics, what drugs fall into the Dipeptidyl peptidase-4 (DPP-4) category?

A

Sitagliptin
Linagliptin
Saxagliptin
Alogliptin

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5
Q

Of the insulin secretagogues used to treat diabetes, there are incretin mimetics and K(ATP) blockers. Of the K(ATP) blockers, what drugs fall into the Sulfonylurea category?

A

First generation:
Chlorpropamide
Tolbutamide
Tolazamide

Second generation:
Glipizide
Glyburide
Glimepiride

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6
Q

Of the insulin secretagogues used to treat diabetes, there are incretin mimetics and K(ATP) blockers. Of the K(ATP) blockers, what drugs fall into the Meglitinide category?

A

Nateglinide

Repaglinide

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7
Q

Biguanide used to tx diabetes

A

Metformin

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8
Q

Thiazolidinediones used to tx diabetes

A

Pioglitazone

Rosiglitazone

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9
Q

Sodium-glucose co-transporter 2 (SGLT2) inhibitors used to tx diabetes

A

Canagliflozin
Dapagliflozin
Empagliflozin

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10
Q

Inhibitors of alpha-glycosidases used to tx diabetes

A

Acarbose

Miglitol

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11
Q

To maintain a state of normoglycemia, insulin helps to decrease blood glucose. What hormones operate in the opposite direction, increasing blood glucose?

A

T3/T4
Glucagon
Epinephrine
Glucocorticoids

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12
Q

Rapid acting insulin is insulin with mutations from human sequence that block assembly of dimers and hexamers, allowing for faster absorption. Onset is within 5-10 mins with duration of 1-3 hrs, with a peak at 30 min to 1 hours. What is the clinical use for rapid acting insulin?

A

Postprandial hyperglycemia — taken before the meal as a SC injection

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13
Q

Short acting and regular insulin consists of unmodified ____ insulin crystals. Absorption rate is _____ and less predictable d/t formation of hexamers that are too bulky to be transported via endothelium into the bloodstream

A

Zinc; slow

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14
Q

Short acting and regular insulin have onset within 30 min-1hr with a duration of 10 hours and peak at 3-5 hours. What are the clinical uses for short acting or regular insulin?

A

Basal insulin maintenance

Overnight coverage

If for prostprandial hyperglycemia, inject 45 min before meal

Can be injected IV in urgent situations

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15
Q

Composition of intermediate acting insulin NPH

A

Complex of protamine with zinc insulin

[protamine has to be digested by tissue proteolytic enzymes before insulin can be absorbed]

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16
Q

NPH is an intermediate-acting insulin with onset in 1-2 hrs, duration 10-12 hrs, and peaks at 4-12 hrs. What are the clinical uses of intermediate acting insulin?

A

Basal insulin maintenance and/or overnight coverage

Use is declining because it is being replaced by long-acting insulin

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17
Q

Difference in composition between long acting insulins: Detemir and Glargine

A

Detemir = Lys 29 in B chain is myristoylated (lipid) — rapidly absorbed into blood but binds strongly to albumin; Detemir peaks at 3-9 hrs.

Glargine = amino acid substitutions in both A and B chains enhance crystal stability, change pKa of insulin — soluble at low pH (4) but precipitates at pH 7; Glargine is “peakless”

Both are used for basal insulin maintenance (1-2 SC injections/day) with onset 3-4 hrs, duration 24 hrs

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18
Q

How is insulin used in the tx of severe hyperkalemia?

A

Insulin + glucose (to prevent hypoglycemic shock) + furosemide

Insulin rapidly activates Na/K ATPase to shift K+ into cells

Effect is transient (several hours); in the meantime K+ is eliminated from the body using loop diuretic

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19
Q

AEs of insulin

A

Hypoglycemia (most common)

Lipodistrophy (localized hypertrophy of subcutaneous fat at site of injection — can be prevented by changing injection site, or using IM injection)

Resistance (pts treated with exogenous insulin commonly develop insulin binding Abs — IgG can neutralize its actions)

Allergic reactions (immediate type HSR)

Hypokalemia

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20
Q

Common causes of hypoglycemia in the setting of insulin therapy

A

Delay of meal or missed meal

Exercise — exercising skeletal muscle consumes more glucose; hyperemic skin —> enhanced rate of insulin absorption

Overdose of insulin

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21
Q

Signs of hypoglycemia

A

Confusion, bizarre behavior, seizures, coma

Sympathetic hyperactivity: tachycardia, palpitations, sweating, tremor

Parasympathetic hyperactivity: hunger, nausea

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22
Q

Tx for hypoglycemia resulting from insulin therapy

A

Glucose (juice, candy, etc. if conscious — if unconscious use IV glucose)

Diazoxide — strong hyperglycemic agent (K+ATP channel opener); inhibits release of insulin by beta cells

Glucagon

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23
Q

Amylin is a pancreatic hormone synthesized by beta cells. Its analog Pramlintide can be used as an adjunct to treat diabetes. What is the MOA?

A

Inhibits glucagon secretion

Enhances insulin sensitivity

Decreases gastric emptying (slows rate of intestinal glucose absorption)

Causes satiety

[rapid onset, 3 hr duration, peak at 20 mins]

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24
Q

Adverse effects of pramlintide

A

Nausea, vomiting, diarrhea, anorexia

Severe hypoglycemia — especially if used together with insulin — insulin dose should be reduced

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25
Q

Drug interactions with pramlintide

A

Enhances effects of anticholinergic drugs in GI tract (i.e., constipation)

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26
Q

Endogenous factors regulating insulin secretion

A

Glucose and other energy substrates

GPCR-G(s) ligands — beta2-AR agonists, GLP-1 receptor agonists (incretins)

GPCR-G(i) ligands — somatostatin, alpha2-AR agonists

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27
Q

_____ are a group of gastrointestinal hormones that cause a decrease in blood glucose levels

A

Incretins

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28
Q

Hormone synthesized by intestinal L-cells that promotes beta-cell proliferation, insulin gene expression, glucose-dependent insulin secretion, and inhibits glucagon secretion; causes sateity and inhibits gastric emptying but is NOT an effective drug d/t short half life

A

GLP-1

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29
Q

Recombinant form of exendin-4, protein from Gila monster saliva with glycine substitution to make it less susceptible to hydrolysis by DPP-4

A

Exenatide

30
Q

GLP-1 analog with 97% homology to native GLP-1, lipid-modified to be rapidly absorbed but binds to albumin

A

Liraglutide

31
Q

Clinical use of GLP-1 receptor agonists

A

The release of GLP-1 is diminished postprandially in T2DM pts —> inadequate glucagon suppression and excess hepatic glucose output

GLP-1 receptor agonists are approved in T2DM pts who are not adequately controlled by metformin/sulfonylureas/thiazolidinediones

Doses of other anti-diabetic meds should be reduced to avoid hypoglycemia

32
Q

AEs of GLP-1 receptor agonists

A

N/V, diarrhea, anorexia

Hypoglycemia (although lower risk than Pramlintide bc exhibits glucose-dependent insulinotropism)

Linked to cases of acute pancreatitis and pancreatic cancer

33
Q

MOA of DPP-4 inhibitors (gliptins)

A

DPP-4 is a serine protease that degrades GLP-1 and other incretins

Increase levels of GLP-1 to enhance its interactions with the cognate receptor — effects are similar to those of GLP-1 agonists

34
Q

Clinical use of DPP-4 inhibitors (gliptins)

A

Approved as adjunctive therapy to diet and exercise in pts with T2DM

Used both as monotherapy and in combo with metformin/sulfonylureas/TZDs

35
Q

AEs of DPP-4 inhibitors (gliptins)

A

URIs and nasopharyngitis

Linked to acute pancreatitis

Hypoglycemia (if combined with insulin secretagogues — their doses have to be adjusted)

36
Q

MOA of K(ATP) channel blockers

A

Binding to SUR — sulfonylurea receptor

Blocking K+ current through Kir6.2 inwardly rectifying potassium channel

37
Q

Clinical use of sulfonylureas

A

T2DM as a monotherapy or in combo with insulin or other anti-diabetic drugs

38
Q

AEs of sulfonylureas

A

Hypoglycemia

Weight gain (increased insulin release)

Secondary failure — pts who respond initially later cease to respond to sulfonylureas and develop unacceptable hyperglycemia

Dermatological and general hypersensitivity reactions — cross-reactivity with other sulfonamidees (sulfonamide abx, carbonic anhydrase inhibitors, diuretics — thiazides, furosemide)

39
Q

Drug interactions of sulfonylureas that enhance their hypoglycemic effect

A

Displacing from binding with plasma proteins: sulfonamides, clofibrate, salicylates

Enhancing the effect on K(ATP) channel: ethanol

Inhibiting CYP enzymes: azole antifungals, gemfibrozil, cimetidine, etc.

40
Q

Drug interactings with sulfonylureas that decrease their glucose-lowering effect

A

Inhibiting insulin secretion: beta blockers, CCBs

Antagonizing their effect on K(ATP) channel: diazoxide

Inducing hepatic CYP enzymes: phenytoin, griseofulvin, rifampin, etc.

41
Q

MOA of meglitinides (repaglinide and nateglinide)

A

K(ATP) channel inhibition —similar to sulfonylureas

42
Q

Clinical use of meglitinides

A

Control of postprandial hyperglycemia in pts with T2DM

Taken orally before the meal; can be used alone (to control postprandial hyperglycemia) or in combo with other antidiabetic drugs

43
Q

AEs of meglitinides

A

Hypoglycemia
Secondary failure
Weight gain

44
Q

MOA of metformin (biguanide)

A

Activation of AMP-dependent protein kinase

AMP-dependent protein kinase phosphorylates a number of targets —> inhibition of lipogenesis and gluconeogenesis, increase in glucose uptake, glycolysis, and FA oxidation, lower glucose levels in hyperglycemic (but not normoglycemic) states, increases insulin sensitivity

[Exact MOA is unclear — may be indirect—inhibition of respiratory complex I in mitochondria]

45
Q

Clinical use for metformin

A

The most commonly used oral agent to tx T2DM and generally accepted as first-line tx

Advantages: superior or equivalent glucose-lowering efficacy compared to other oral meds, does not cause hypoglycemia, does not cause weight gain, taken orally, can be used either alone or in combo with other oral agents, in clinical trials decreased the risk of both macro-and microvascular complications in diabetic pts

46
Q

Pharmacokinetics of metformin

A

Half life 1.5-3 h

Not bound to plasma proteins

Not metabolized; excreted unchanged by kidneys

47
Q

AEs of metformin

A

Most common are GI complications — anorexia, vomiting, nausea, diarrhea, and abdominal discomfort

Decreased absorption of Vit B12

Lactic acidosis, especially under conditions of hypoxia, renal, and hepatic insufficiency

48
Q

Contraindications to metformin

A

Contraindicated in conditions predisposing to tissue hypoxia (HF, COPD), renal failure, chronic alcoholism and cirrhosis

49
Q

MOA of thiazolidinediones (pioglitazone, rosiglitazone)

A

Ligands of peroxisome proliferator-activated receptor-gamma (PPARy)

PPARy is a nuclear receptor expressed primarily in fat, muscle, liver tissue, and endothelium

Leads to increased GLUT4 in skeletal m. and adipocytes; increased IRS1, IRS2, and PI3K; decreased PEPCK, NF-kB, and AP-1

50
Q

Thiazolidinediones are taken orally once daily, and since their effects are d/t changes in gene expression their onset is delayed 1-3 months. How are they metabolized? Are they safe in renal failure pts?

A

Metabolized by the liver — half life is reduced by CYP inducers (rifampin) and prolonged by CYP inhibitors (gemfibrozil)

YES safe to administer in renal failure

51
Q

Clinical use of thiazolidinediones

A

T2DM, alone or in combo with other antidiabetic drugs

Shown to delay progression from prediabetes to T2DM

Euglycemic drugs (no hypoglycemia when used alone)

52
Q

AEs of thiazolidinediones

A

Weight gain and edema (increased risk if administered with insulin)

[edema may be d/t increase in vascular permeability and/or increase in ENaC expression — thus increasing sodium and water reabsorption in collecting duct]

Exacerbation of heart failure (contraindicated in class III or IV HF pts)

Increased TC and LDL-C (rosiglitazone)

Osteoporosis (direct MSCs to adipocyte differentiation so less osteoblast lineage)

53
Q

MOA of sodium-glucose co-transporter2 inhibitors

A

Glucose is reabsorbed in proximal tubule primarily by SGLT2

Gliflozins inhibit this transporter to increase glucose excretion and reduce hyperglycemia

Other effects: causes osmotic diuresis, induces weight loss, reduces BP, reduces plasma uric acid levels, does not cause hypoglycemia when used alone

54
Q

Clinical use of SGLT2 inhibitors

A

As an adjunct to diet and exercise in adults with T2DM

Taken orally before first meal once/day

In pts with hypovolemia, this condition should be correct prior to starting therapy

55
Q

AEs of SGLT2 inhibitors

A

Hypotension

Hypovolemia

Genital (mycotic) and urinary tract infections

Hypoglycemia if combined with insulin or insulin secretagogues

Renal function impairment — induce fall in GFR

Hyperkalemia (esp in pts with impaired renal function and those taking ACEIs, ARBs, and K-sparing drugs)

56
Q

MOA of alpha-glycosidase inhibitors (acarbose, miglitol)

A

Only monosaccharides are absorbed from GI into blood

Competitive inhibition of alpha-glycosidases (family of enzymes on intestinal epithelium) defer digestion and thus absorption of ingested starch and disaccharides

Lower postprandial hyperglycemia to create an insulin-sparing effect

57
Q

Clinical use of alpha-glycosidase inhibitors

A

T2DM as monotherapy or in combo with other oral antidiabetic agents or insulin

Taken orally at mealtime, do not cause hypoglycemia when used alone, do not cause weight gain

58
Q

AEs of alpha-glycosidase inhibitors

A

Most common are malabsorption, flatulence, diarrhea, and abdominal bloating

Hypoglycemia has been described when combined with insulin or insulin secretagogues

59
Q

Drug interactions with alpha glycosidase inhibitors

A

Decrease absorption of digoxin (acarbose) and propranalol and ranitidine (miglitol)

60
Q

A 24 y/o 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 lispro and insulin aspart
B. Evening injections of mixed regular insulin and insulin glargine
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

Insulin glargine covers long-term release, lispro (short-acting) covers postprandial hyperglycemia

61
Q

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

A. Glucose binds GLUT transporter; depolarization; increase in cell ATP, calcium channel closes
B. Glucose binds to the GLUT transporter; increase in cell ATP; potassium channel closes, depolarization
C. Glucose binds GLUT transporter; potassium channel opens, increase in intracellular calcium
D. Glucose binds GLUT transporter; potassium channel closes; depolarization; decrease in intracellular calcium
E. Glucose binds GLUT transporter; potassium channel closes; hyperpolarization; increase in intracellular calcium

A

B. Glucose binds GLUT transporter; increase in cell ATP; potassium channel closes; depolarization

62
Q

Which of the following will increase the release of insulin by islet beta cells?

A. Clonidine
B. Verapamil
C. Isoproterenol
D. Somatostatin
E. Atenolol
A

C. Isoproterenol
[beta1 and beta 2 mimetic — increases release of insulin]

Clonidine is an alpha2 agonist — will decrease insulin release

Verapamil is calcium channel blocker — will decrease insulin release

63
Q

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

A. Metformin
B. Insulin
C. Pramlintide
D. Repaglinide

A

D. Repaglinide

All these will decrease hypoglycemia but only one that does so via stimulating insulin secretion is Repaglinide (a meglitinide in the K[ATP] channel blocking class)

64
Q

18 y/o patient presents with signs and symptoms that suggest T1DM. What is the tx plan?

A. Metformin
B. Glyburide
C. Lifestyle adjustments only
D. Insulin
E. Reosiglitazone
A

D. Insulin

65
Q

Type 1 diabetic patient is started on insulin. Which of the following is appropriate regimen?

A. Pre-meal detamir and lispro at bedtime
B. Pre-meal lispro and glulisine after daily exercise
C. Pre-meal aspart and glargine at bedtime
D. Lispro QD before bed
E. Glulisine QD in the morning

A

C. Pre-meal aspart and glargine at bedtime

66
Q

Which of the following sets glargine apart from other formulations?

A. Blood levels and hypoglycemic effects more accurately described as plateau rather than definite spike or peak
B. Disulfiram-like effect more common and severe
C. Fast onset of action and useful for postprandial hyperglycemia
D. Poses little or no risk of hypoglycemia if pt skips meals
E. Sensitizes parenchymal cells to insulin

A

A. Blood levels and hypoglycemic effects more accurately described as plateau rather than definite spike or peak

67
Q

Which of the following is most appropriate in a pt who presents with lethargy, moderate ketonemia, and BG of 450?

A. Glyburide
B. Metformin
C. Insulin aspart
D. Insulin regular
E. Insulin glargine
A

D. Insulin regular

This is urgent situation that requires IV insulin, and the only insulin formulation that can be given IV is regular insulin

68
Q

Which of the following does not cause increased risk of weight gain?

A. Canagliflozin
B. Insulin
C. Glipizide
D. Pioglitazone
E. Repaglinide
A

A. Canagliflozin
[an SGLT2 inhibitor]

T2D pts who are obese should avoid insulin, TZDs, sulfonylureas, and meglitinides. They tend to lose weight on biguanides, SGLT2 inhibitors, GLP-1 agonists, and DPP-4 inhibitors

69
Q

Which of the following is associated with increased risk of lactic acidosis?

A. Acarbose
B. Glyburide
C. Metformin
D. Insulin
E. Liraglutide
A

C. Metformin

[increased risk of lactic acidosis especially under conditions of hypoxia, renal, and hepatic insufficiency]

70
Q

How would a type 1 diabetic’s insulin therapy regimen be adjusted if pt is placed on prednisolone therapy?

A. Add glyburide
B. Add glucagon
C. Cancel insulin and start metformin
D. Decrease insulin dose
E. Increase insulin dose
A

E. Increase insulin dose

71
Q

How should glyburide dose be adjusted in a pt that has been prescribed sulfa abx for a UTI?

A. Increase glyburide dose
B. Decrease glyburide dose
C. No change in glyburide dose

A

B. Decrease glyburide dose

Endo Repro Exam II (28 decks)

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