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Endocrine Pharm > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Four factors that increase insulin release

A

Glucose, sulfonylureas, M-agonists, B2-agonist

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2
Q

IV forms of insulin

A

Lispro and regular

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3
Q

Long-acting insulin with no peak

A

Glargine

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4
Q

Mechanism of action: Insulin

A

binds transmembrane receptors–>tyrosine kinase–> phosphorylate tissue-specific substrates

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5
Q

Does a-2 agonist cause hyper- or hypoglycemia

A

↓ insulin resistance–>hyperglycemia

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6
Q

Symptoms of DKA

A

polyuria, polydipsia, nausea, fatigue, dehydration, Kussmaul breathing, fruity breath

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7
Q

Symptoms of hypoglycemia

A

lip/tongue tingling, lethargy, confusion, sweats, tremors, tachycardia, coma, seizures

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8
Q

Mechanism of action: Glucose

A

Enters Beta cell via GLUT2–> glycolysis produces ATP–> ATP closes K channels–> cell depolarizes–> Ca channels open–> insulin release

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9
Q

Mechanism of action: Sulfonylureas

A

Blocks K channels–> depolarization–> insulin release, ↓glucagon release and ↑insulin receptor sensitivity

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10
Q

First generation oral sulfonylureas (OSU)

A

Acetohexamide, Tolbutamide, Chlorpropamide

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11
Q

Acetohexamide: Class and unique properties

A

FG OSU; active metabolite (long duration), need to ↓ dose in renal dysfxn

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12
Q

Tolbutamide: Class and unique properties

A

FG OSU; appropriate in renal dysfxn

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13
Q

Chlorpropamide: Class and unique properties

A

long-acting, SIADH/disulfiram reactions

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14
Q

Second generation OSU

A

Glipizide and Glyburide

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15
Q

Glipizide: Class and unique properties

A

need to ↓ dose in hepatic dysfuntion

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16
Q

Glyburide: Class and unique properties

A

active metabolite, need to ↓ dose in renal dysfunction

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17
Q

SE’s of OSU’s

A

hypoglycemia, weight gain, drug interactions w/cimetidine, insulin, salicylates and sulfonamides

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18
Q

Mechanism of action: Metformin

A

bypasses insulin receptor–> directly into cell–> stim PPAR and inhibits mitochondrial glycerophosphate dehydrogenase–> ↑ tissue sensitivity to insulin and ↓ liver gluconeogensis

19
Q

SE’s of Metformin

A

possible lactic acidosis, GI distress; CI in CHF. NO weight or hypoglycemia

20
Q

Mechanism of action: Acarbose & Miglitol

A

inhibits a-glucosidase in SI–>↓ breakdown of glucose to absorbable carb–>↓ postprandial glucose–> ↓insulin demand. NO HYPOGLYCEMIA

21
Q

SE’s of Acarbose & Miglitol

A

GI discomfort, flatulence, diarrhea, hepatotoxicity

22
Q

Thiazolidinediones

A

Pioglitazone and Rosiglitazone

23
Q

Mechanism of action: Thiazolidinediones

A

bind to nuclear PPARy–> transcription of insulin-responsive genes–> sensitization of tissues to insulin, ↓hepatic gluconeogenesis and TGs, and ↑insulin receptor numbers

24
Q

SE’s of Thiazolidinediones

A

GOOD: less hypoglycemia than sulfonylureas, ↓TG ↑HDL

BAD: weight gain, bone fractures, increased bladder cancer and edema; CI in CHF; Rosiglitazone ↑ LDL

25
Q

Mechanism of action: Exenatide

A

GLP-1 receptor agonist; GLP-1 ↑glucose-dependent insulin secretion, ↓glucagon secretion, slows gastric emptying, ↑satiety; used in type 2 diabetes in combo w/other

26
Q

SE’s of Exenatide

A

nausea, hypoglycemia w/sulfonylureas, acute pancreatitis, caution w/renal insufficiency

27
Q

Mechanism of action: Sitagliptin

A

inhibits DPP-4 (which normally inactivates GLP-1)

28
Q

Mechanism of action: Repaglinide and Nateglinide

A

Closes K channels–>stimulates insulin release; T2DM

29
Q

Mechanism of action: Pramlintide

A

slows rate of food absorption–> ↓glucose production and ↓appetite; T1DM and T2DM

30
Q

Meglitinides: Drug types and SE’s

A

Repaglinide and Nateglinide; weight gain, hypoglycemia, very short acting

31
Q

Other GLP-1 Receptors agonists

A

Liraglutide, Albiglutide, Dulaglutide

32
Q

Other DPP-4 inhibitors

A

Alogliptin, Saxagliptin, Linagliptin

33
Q

SE’s of DPP-4 inhibitors

A

Some urticaria/angioedema; URIs, headace; some pancreatitis; weight neutral, no hypoglycemia

34
Q

Sodium glucose cotransporter 2 (SGLT2) inhibitors

A

Canagliflozin, Dapaglifozin, Empagliflozin

35
Q

Mechanism of action: SGLT2 inhibitors

A

↓ glucose resorption in kidney–>↑ urinary glucose excretion

36
Q

SE’s of SGLT2 inhibitors

A

Volume depletion, hyperkalemia; UTI’s, genital infections; ↑LDL; no weight gain or hypoglycemia

37
Q

Bile acid sequestrant

A

Colesevelam

38
Q

Mechanism of action: Colesevelam

A

binds bile acid/cholesterol–> ↓hepatic glucose production; NO hypoglycemia, ↓LDL

39
Q

SE’s of Colesevelam

A

Constipation, ↑TGs

40
Q

Rapidly acting insulins (3)

A

Lispro, Aspart, Glulisine

41
Q

Short acting insulin

A

Regular insulin

42
Q

Intermediate acting insulins (4)

A

NPH, NPL, NPA and Detemir

43
Q

SE’s of GLP-1 agonists

A

GOOD: weight reduction
BAD: hypoglycemia, NVD, acute pancreatitis, C-cell hyperplasia/medullary thyroid CA

Endocrine Pharm (7 decks)

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