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E2T1 > Diabetes Drugs DSA > Flashcards

Diabetes Drugs DSA Flashcards

1
Q

drugs used in diabetes

A
  • insulins
  • amylin analog
  • insulin secretagogues
  • biguanides
  • thiazolidinediones
  • sodium-glucose co-transporter 2
  • inhibitors of alpha-glycosidases
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2
Q

Insulins- rapid acting

A

-Aspart
-Lispro
-Glulisine
(ALG)

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3
Q

Insulins- short-acting

A

-regular insulin

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4
Q

insulins- intermediate-acting

A

-NPH

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5
Q

insulins- long-acting

A
  • Detemir

- Glargine

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6
Q

insulin- moa

A
  • IR-IRS-P13K-Akt pathway- effects on glucose, lipid and protein metabolism, primarily via reg of enzyme activities
  • IR-IRS-MAP kinases- reg of gene transcription and cell proliferation
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7
Q

effects of insulin- gene expression

A
  • ELK1 (ETS family of TFs)
  • AP-1 TF
  • FoxO1 (forkhead TFs)
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8
Q

insulin- ELK1

A
  • IR-IRS-Ras-Raf-MEK-ERK-inc ELK1!
  • cell growth and diff
  • cell prolif and inc survival
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9
Q

insulin- AP-1 TF

A
  • IR-IRS-P1-3K-Rac-inc JNK- inc AP-1
  • cell growth and diff
  • cell prolif and apoptosis
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10
Q

Insulin- FoxO1

A
  • IR-IRS-Pl-2K- Akt- dec FoxO1
  • inc PPAR-y expression and lipogenesis
  • dec glycogenolysis
  • dec gluconeogenesis
  • enhanced cell diff
  • escaping cell cycle arrest and inc prolif
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11
Q

insulin- carbohydrate metabolism

A
  • glucose transport- GLUT4 translocation to cell membrane (skeletal m, cardiac myocytes, adipocytes)
  • act of glycolysis
  • act of glycogen syn
  • inhibition of gluconeogenesis
  • inhibition of glycogenolysis
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12
Q

Insulin- lipid metabolism

A
  • inhibition of lipolysis

- enhanced lipogenesis

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13
Q

insulin- protein metabolism

A

-inc prot synthesis

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14
Q

Rapid acting insulins- clinical use

A

(Aspart, Lispro, Glulisine)

  • postprandial hyperglycemia- take before meal
  • onset 5-10 min
  • duration 1-3 hrs
  • peak 30 min -1 hr
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15
Q

short-acting insulin- clinical use

A

(regular insulin)

  • composition- unmodified zinc insulin crystals
  • absorption rate is slow and less predictable
  • basal insulin maintenace; overnight coverage; postprandial hyperglycemia (45 min b/f meal)
  • onset 30 m - 1 hr
  • duration 10 hrs
  • peak 3-5 hrs
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16
Q

Intermediate acting insulin

A

(NPH)

  • complex of protamine with zinc insulin- protamine has to be digested by tissue proteolytic enzymes b/f insulin can be absorbed
  • basal insulin maintenance and/or overnight coverage
  • use is declining- replaced by long-acting insulins
  • onset 1-2 h
  • duration 10-12 h
  • peak 4-12 h
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17
Q

long-acting isulin- clinical use

A

(Detemir, Glargine)

  • basal insulin maintenance (1-2 injections dialy)
  • onset 3-4 h
  • duration 24 h
  • peak 3-9 h (detemir); peakless (glargine)
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18
Q

clinical indications for insulin

A
  • type 1 diabetes
  • type 2 diabetes (inadequately controlled by diet, exercise, and non-insulin tx)
  • gestational diabetes
  • severe hyperkalemia- insulin + glucose + furosemide- act Na/K-ATPase- shift K from extracellular fluid into cells
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19
Q

insulin- adverse effects

A
  • hypoglycemia
  • lipodystrophy- hypertrophy/atrophy of subcutaneous fat at site of injection- prevented by freq changing the site of injection
  • resistance- insulin binding ab’s (IgG)
  • allergic rxns (rare- histamine release from mast cells)
  • hypokalemia
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20
Q

most common complication of insulin therapy; caused by?

A

hypoglycemia!!

  • delay of a meal/missed meal
  • exercise
  • overdose of insulin
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21
Q

signs of hypoglycemia

A
  • CNS/behavioral sx- confusion, bizarre behavior, seizures, coma
  • symp hyperactivity- tachycardia, palpitations, sweating, tremor
  • parasymp hyperactivity- hunger, nausea
  • pts on tight glycemic control- “hypoglycemic unawareness”
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22
Q

hypoglycemia- tx

A
  • glucose!- juice, candy (if conscious), IV glucose (if unconscious)
  • diazoxide- Katp channel opener- inhibits the release of insulin by B cells
  • glucagon
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23
Q

glucagon- moa

A

Gs-coupled GPCR

  • act of AC
  • act of PKA
  • act of phosphorylase–> glycogenolysis
  • inc expression of PEPCK and G6Pase- gluconeogenesis
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24
Q

Glucagon- effects

A
  • hepatocytes- inc glucose output, glycogen depletion
  • potent inotropic and chronotropic effect on heart
  • GI smooth m relaxation
  • inc insulin release by B-cells
  • inc release of catecholamines by chromaffin cells (contraindicated in pheochromocytoma pts)
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25
Q

glucagon- clinical uses

A
  • moderate/severe hypoglycemia
  • B-blocker overdose
  • radiology of bowel
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26
Q

Amylin analog

A

-pramlintide

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27
Q

amylin analog- clinical use

A
  • type 1 diabetes
  • type 2 diabetes who takes mealtime insulin therapy
  • injected sc b/f meals as an adjunct to insulin therapy
28
Q

amylin analog- adverse effects

A
  • GI- N/V, diarrhea, anorexia

- severe hypoglycemia (if used with insulin, insulin dose should be reduced)

29
Q

amylin analog- drug interactions

A

-enhances effects of anticholinergic drugs in GI tract (constipation)

30
Q

insulin secretagogues

A
  • incretin mimetics- GLP-1 agonists, DPP-4 inhibitors

- KATP channel blockers- sulfonylureas, meglitinides

31
Q

GLP-1 agonists

A

-exenatide
-liraglutide
(EL)

32
Q

GLP-1 agonists- clinical use

A
  • release of GLP-1 is diminished postprandially in type 2 diabetes pts- inadequate glucagon suppression and excessive hepatic glucose output
  • approved for type 2 diabetes pts who arent controlled by metformin/sulfonylureas/thiazolidinediones
  • doses of other anti-diabetic meds should be reduced
  • parenteral route- improved control of hyperglycemia, induce weight loss
33
Q

GLP-1 agonists- adverse effects

A
  • GI- N/V, diarrhea, anorexia
  • lower risk of hypoglycemia vs pramlintide
  • linked to acute pancreatitis and pancreatic cancer
  • linked to thyroid cancer
34
Q

DPP-4 (dipeptidyl peptidase-4) inhibitors

A

-Sitagliptin
-Linagliptin
-Saxagliptin
-Alogliptin
(gliptins)

35
Q

DPP-4 inhibitors- moa

A

-serine protease that degrades GLP-1 and other incretins

36
Q

DPP-4 inhibitors- clinical use

A
  • adjunctive tx to diet and exercise in pts with type 2 diabetes
  • monotherapy or with metformin/sulfonylureas/TZDs
  • orally!
37
Q

DPP-4 inhibitors- adverse effects

A
  • URIs and nasopharyngitis
  • acute pancreatitis
  • hypoglycemia (if combined with insulin secretagogues- doses must be adjusted)
38
Q

Sulfonylureas- first generation

A

-chlorpropamide
-tolbutamide
-tolazamide
(CTT)

39
Q

Sulfonylureas- second generation

A
  • glipizide
  • glyburide
  • glimepiride
40
Q

Meglitinides

A
  • Nateglinide

- Repaglinide

41
Q

Sulfonylureas- clinical use

A

-type 2 diabetes as a monotherapy or in combi with insulin or other anti-diabetic drugs

42
Q

sulfonylureas- adverse effects

A
  • hypoglycemia
  • weight gain
  • secondary failure- respond initially, later cease to respond- develop unacceptable hyperglycemia
  • disulfiram-like effect of alcohol-induced flushing
  • dermatological and general hypersensitivity rxns- cross-reactivity with other sulfonamides (abx, carbonic anhydrase inb, diuretics- thiazides, furosemide)
43
Q

sulfonylureas- drug interactions- enhancing their hypoglycemic effect

A
  • displacing from binding with plasma proteins- sulfonamides, clofibrate, salicylates
  • enhance the effect on KATP channel- ethanol
  • inhibit CYP enzymes- azole antifungals, gemfibrozil, cimetidine
44
Q

sulfonylureas- drug interactions- dec their glucose-lowering effect

A
  • inhibit insulin secretion- B-blockers, CCBs
  • antagonist their effect on KATP channel- diazoxide
  • induce hepatic CYP enzymes- phenytoin, griseofulvin, rifampin
45
Q

Meglitinides- moa

A

-KATP channel inhibition

46
Q

Meglitinides- clinical use, SE’s

A
  • postprandial hyperglycemia in pts with type 2 diabetes
  • orally before meal
  • alone or in combo with other antidiabetic drugs
  • hypoglycemia, secondary failure, weight gain
47
Q

Biguanides

A

-metformin

48
Q

Metformin- moa

A
  • act of AMP-dep protein kinase
  • inhibition of lipogenesis and gluconeogenesis
  • inc in glucose uptake, glycolysis, fatty acid oxidation
  • lower glucose levels in hyperglycemic state
  • inc insulin sensitivity
49
Q

metformin- clinical use, advantages

A

most commonly used oral agent to treat type 2 diabetes!!!- first-line tx!!

  • superior/equivalent glucose-lowering efficacy compared to other oral meds
  • doesnt cause hypoglycemia or weight gain
  • taken orally
  • dec risk of macro and micro-vascular complications in diabetic pts
50
Q

metformin- adverse effects, contraindications

A
  • GI
  • dec abs of B12
  • lactic acidosis- esp under conditions of hypoxia, renal and hepatic insuff
  • contraindicated in conditions predisposing to tissue hypoxia (HF, COPD), renal failure, chronic alcoholism, cirrhosis
51
Q

Thiazolidinediones

A
  • pioglitazone

- rosiglitazone

52
Q

Thiazolidinediones- moa

A
  • ligands of PPARy (proliferator-activated R-gamma)
  • endogenous ligands- prostaglandins and free fa’s
  • TZDs have a much higher affinity for PPARy- bind and go to to R and target it to nucleus- gene expression:
  • inc GLUT4 in skeletal m- enhances glucose uptake, reduced hyperglycemia
  • inc GLUT4 in adipocytes
  • inc insulin sensitivity
  • inc adiponectin- inc insulin sensitivity and dec infl
  • dec PEPCK- inhibit gluconeogenesis
  • dec NF-kB and AP-1 transactivation- dec prod of cytokines
53
Q

Thiazolidinediones- pharmacokinetics

A
  • taken orally once daily
  • onset is delayed- full effect after 1-3 months
  • metabolized by liver
54
Q

Thiazolidinediones- clinical use

A
  • type 2 diabetes- alone or in combo
  • delay progression from prediabetes to type2 diabetes
  • euglycemic drugs (no hypoglycemia when used alone)
55
Q

Thiazolidinediones- adverse effects

A
  • weight gain
  • edema
  • linkto inc risk of bladder cancer
  • osteoporosis
  • inc TC and LDL-C
56
Q

SGLT2 (sodium-glucose co-transporter 2) inhibitors

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
57
Q

SGLT2 inhibitors- moa

A
  • kidneys filter 160-180 g of glucose/day- glucose reabs in proximal tubule by SGLT2
  • inhibit SGLT2 to inc glucose excretion and to reduce hyperglycemia
58
Q

SGLT2 inhibitors- other effects

A
  • osmotic diuresis
  • weight loss
  • reduce BP
  • reduce plasma levels of uric acid
  • doesnt cause hypoglycemia when used alone
59
Q

SGLT2 inhibitors- clinical use

A
  • adjunct to diet and exercise in type 2 diabetic pts
  • taken orally b/f first meal once a day
  • in pts with hypovolemia- should be corrected first b/f start of therapy
60
Q

SGLT2 inhibitors- adverse effects

A

-hypotension
-hypovolemia
-genital and UTIs- can lead to life-threatening blood and kidney infections
-hypoglycemia
-inc LDL-C
renal fxn impairment
-hyperkalemia
-ketoacidosis

61
Q

Inhibitors of alpha-glycosidases

A
  • acarbose

- miglitol

62
Q

Inhibitors of alpha-glycosidases- moa

A
  • inhibition of alpha-glycosidases (located on brush border of intestinal epit)
  • only monosaccharides are absorbed from GI into the blood
  • inhibition defer digestion and thus abs of ingested starch and disaccharides
  • lower postprandial hyperglycemia to create an insulin-sparing effect
63
Q

Inhibitors of alpha-glycosidases- clinical use

A
  • type 2 diabetes- monotherapy or combo
  • taken orally at mealtime
  • dont cause hypoglycemia when used alone
  • dont cause weight gain
64
Q

Inhibitors of alpha-glycosidases- adverse effects

A
  • malabs, flatulence, diarrhea, abd bloating

- hypoglycemia when combined

65
Q

Inhibitors of alpha-glycosidases- drug interactions

A

-dec abs of digoxin and propranolol and ranitidine

E2T1 (6 decks)

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