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Diabetes Drugs DSA Flashcards

(65 cards)

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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
glucagon- clinical uses
- moderate/severe hypoglycemia - B-blocker overdose - radiology of bowel
26
Amylin analog
-pramlintide
27
amylin analog- clinical use
- type 1 diabetes - type 2 diabetes who takes mealtime insulin therapy - injected sc b/f meals as an adjunct to insulin therapy
28
amylin analog- adverse effects
- GI- N/V, diarrhea, anorexia | - severe hypoglycemia (if used with insulin, insulin dose should be reduced)
29
amylin analog- drug interactions
-enhances effects of anticholinergic drugs in GI tract (constipation)
30
insulin secretagogues
- incretin mimetics- GLP-1 agonists, DPP-4 inhibitors | - KATP channel blockers- sulfonylureas, meglitinides
31
GLP-1 agonists
-exenatide -liraglutide (EL)
32
GLP-1 agonists- clinical use
- 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
GLP-1 agonists- adverse effects
- GI- N/V, diarrhea, anorexia - lower risk of hypoglycemia vs pramlintide - linked to acute pancreatitis and pancreatic cancer - linked to thyroid cancer
34
DPP-4 (dipeptidyl peptidase-4) inhibitors
-Sitagliptin -Linagliptin -Saxagliptin -Alogliptin (gliptins)
35
DPP-4 inhibitors- moa
-serine protease that degrades GLP-1 and other incretins
36
DPP-4 inhibitors- clinical use
- adjunctive tx to diet and exercise in pts with type 2 diabetes - monotherapy or with metformin/sulfonylureas/TZDs - orally!
37
DPP-4 inhibitors- adverse effects
- URIs and nasopharyngitis - acute pancreatitis - hypoglycemia (if combined with insulin secretagogues- doses must be adjusted)
38
Sulfonylureas- first generation
-chlorpropamide -tolbutamide -tolazamide (CTT)
39
Sulfonylureas- second generation
- glipizide - glyburide - glimepiride
40
Meglitinides
- Nateglinide | - Repaglinide
41
Sulfonylureas- clinical use
-type 2 diabetes as a monotherapy or in combi with insulin or other anti-diabetic drugs
42
sulfonylureas- adverse effects
- 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
sulfonylureas- drug interactions- enhancing their hypoglycemic effect
- displacing from binding with plasma proteins- sulfonamides, clofibrate, salicylates - enhance the effect on KATP channel- ethanol - inhibit CYP enzymes- azole antifungals, gemfibrozil, cimetidine
44
sulfonylureas- drug interactions- dec their glucose-lowering effect
- inhibit insulin secretion- B-blockers, CCBs - antagonist their effect on KATP channel- diazoxide - induce hepatic CYP enzymes- phenytoin, griseofulvin, rifampin
45
Meglitinides- moa
-KATP channel inhibition
46
Meglitinides- clinical use, SE's
- 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
Biguanides
-metformin
48
Metformin- moa
- 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
metformin- clinical use, advantages
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
metformin- adverse effects, contraindications
- 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
Thiazolidinediones
- pioglitazone | - rosiglitazone
52
Thiazolidinediones- moa
- 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
Thiazolidinediones- pharmacokinetics
- taken orally once daily - onset is delayed- full effect after 1-3 months - metabolized by liver
54
Thiazolidinediones- clinical use
- type 2 diabetes- alone or in combo - delay progression from prediabetes to type2 diabetes - euglycemic drugs (no hypoglycemia when used alone)
55
Thiazolidinediones- adverse effects
- weight gain - edema - linkto inc risk of bladder cancer - osteoporosis - inc TC and LDL-C
56
SGLT2 (sodium-glucose co-transporter 2) inhibitors
- Canagliflozin - Dapagliflozin - Empagliflozin
57
SGLT2 inhibitors- moa
- 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
SGLT2 inhibitors- other effects
- osmotic diuresis - weight loss - reduce BP - reduce plasma levels of uric acid - doesnt cause hypoglycemia when used alone
59
SGLT2 inhibitors- clinical use
- 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
SGLT2 inhibitors- adverse effects
-hypotension -hypovolemia -genital and UTIs- can lead to life-threatening blood and kidney infections -hypoglycemia -inc LDL-C renal fxn impairment -hyperkalemia -ketoacidosis
61
Inhibitors of alpha-glycosidases
- acarbose | - miglitol
62
Inhibitors of alpha-glycosidases- moa
- 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
Inhibitors of alpha-glycosidases- clinical use
- type 2 diabetes- monotherapy or combo - taken orally at mealtime - dont cause hypoglycemia when used alone - dont cause weight gain
64
Inhibitors of alpha-glycosidases- adverse effects
- malabs, flatulence, diarrhea, abd bloating | - hypoglycemia when combined
65
Inhibitors of alpha-glycosidases- drug interactions
-dec abs of digoxin and propranolol and ranitidine

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