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RE Pharm > Drugs used in Diabetes- Konorev > Flashcards

Drugs used in Diabetes- Konorev Flashcards

1
Q

What dx criteria for diabetes?

A

increased plasma glucose levels (fasting levels over 125 mg/dl glucose)

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2
Q

What increases blood glucose? (4)

A
  1. T3/T4
  2. Glucagon
  3. Epinephrine
  4. Glucocorticoids
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3
Q

What decrease blood glucose?

A

Insulin

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4
Q

Loss of insulin or insulin responsiveness causes what?

A

Hyperglycemia

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5
Q

Unopposed mobilization of glucose by T3/T4, glucagon, epinephrine, or glucocorticoids causes what?

A

Hyperglycemia

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6
Q

What does insulin receptor MAP kinase pathway do?

A

Regulation of gene transcription and cell proliferation

-Cell growth, proliferation, and gene expression

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7
Q

What does insulin receptor PI3K-Akt pathway do?

A

Regulation of enzyme activities or gene expression to affect metabolism of glucose, lipids, and proteins

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8
Q

How does insulin affect carbohydrate metabolism?

A

Promotes intracellular glucose transport and utilization

  • GLIT4 translocation in skeletal muscle, cardiac myocytes and adipocytes
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9
Q

What are the 2 pathways for the insulin receptor?

A
  1. Insulin receptor -PI-3K-Akt pathway

2. Insulin receptor -MAP kinase pathway

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10
Q

What is the Insulin MAP kinase pathway?

A

promotes cell growth and proliferation gene expression

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11
Q

What is the PI-3K signaling pathway? (2)

A

1.synthesis of lipids, proteins, and glycogen

2 GLUT-4 expression on cell membrane

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12
Q

What are the anabolic effects of insulin on carbohydrate metabolism? (3)

A

Promotes intracellular glucose transport and utilization

  1. GLUT4 translocation to the cell membrane in skeletal muscle, cardiac myocytes, and adipocytes
  2. Activation of glycolysis
  3. Activation of glycogen synthesis
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13
Q

What processes does insulin oppose?(2)

A
  1. Inhibition of gluconeogenesis

2. Inhibition of glycogenolysis

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14
Q

What type of drugs are aspart, lispro and glulisine?

A

Rapid acting insulins

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15
Q

What is aspart?

A

rapid acting insulin

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16
Q

What is lispro?

A

rapid acting insulin

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17
Q

What is Glulisine?

A

rapid acting insulin

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18
Q

What is regular insulin?

A

short acting insulin

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19
Q

What type of drug is determir and glargine

A

long acting insulin

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20
Q

What is the clinical use of Rapid-acting Insulin (Aspart, Lispro, Glulisine)

A

Postprandial hyperglycemia

- taken before the meal as sc injections only

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21
Q

What is the onset, duration, peak of Rapid-acting insulin (Aspart Lispro Glulisine)

A

Onset:5-10min
• Duration: 1-3 hr
• Peak: 30 min-1 hr

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22
Q

What is clinical application of short acting regular insulin?(4)

A
  1. Basal insulin maintenance
  2. Overnight coverage
  3. If for postprandial hyperglycemia – inject 45 min before the meal
  4. Can be injected intravenously in urgent situations
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23
Q

What is Neutral protamine Hagdorn?

A

An intermediate insulin complexed with protamine that can’t be absorbed

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24
Q

What is the onset, duration, peak regular insulin?

A
  1. Onset: 30 min-1 hr
  2. Duration: 10 hr
  3. Peak: 3-5 hr
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25
Q

What is use of intermediate acting insulin Neutral protamine Hagdorn?

A
  1. Basal insulin maintenance and/or overnight coverage

2. Use is declining – is being replaced by long-acting insulins

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26
Q

What is onset, duration, and peak of Neutral protamine Hagdorn?

A
  • Onset:1-2hr
  • Duration: 10-12 hr
  • Peak: 4-12 hr
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27
Q

What is the use of long acting insulins Detemir and glargine?

A

Basal insulin maintenance 1-2 sc injections daily

-Onset: 3-4 hr
-Duration: 24hr
Peak: Detemir 3-9 hr; Glargine (no peak)

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28
Q

Why is the tight glycemic control provided by insulins necessary? (3)

A
  1. Improves survival
  2. Reduces diabetic complications
  3. Has been shown to be effective in multiple clinical trials, especially in patients with type 1 diabetes
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29
Q

How does insulin treat severe hyperkalemia? (4)

A
  1. Insulin + glucose (to prevent hypoglycemic shock) + furosemide
  2. Insulin (i.v.) rapidly activates Na+/K+-ATPase to shift K+ from extracellular fluid into cells
  3. Effect is transient (several hours)
  4. K+ is eliminated from the body using loop diuretics in the meantime
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30
Q

What are adverse effects of insulin? (5)

A

HLARH

  1. Hypoglycemia
  2. Lipodistrophy–> hypertrophy of fat at injection site
  3. Allergic reactions–> immediate HS is rare
  4. Resistance–> insulin binding antibodies may cause resistance
  5. Hypokalemia
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31
Q

– CNS/Behavioral Manifestations: confusion, bizarre behavior, seizures, coma

– Sympathetic hyperactivity: tachycardia, palpitations, sweating, tremor

– Parasympathetic hyperactivity: hunger, nausea

are complications of what?

A

Hypoglycemia–> most common complications of insulin therapy

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32
Q

What is the treatment for hypoglycemia?

A
  1. Glucose or sucrose

2. SQ glucagon

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33
Q

What is amylin analog?

A

analog of amylin, pancreatic hormone synthesized by beta cells that enhances the action of insulin

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34
Q

How does amylin enhance the action of insulin?

A
  1. Inhibition of glucagon secretion
  2. Decreased gastric emptying (slows the rate of intestinal glucose absorption)
  3. Causes a feeling of satiety
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35
Q

What is pramlintide?

A

Amylin analog drug (pancreatic hormone synthesized by beta cells that enhances the action of insulin )

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36
Q

What its the clinical use of pramlintide?(3)

A
  1. Type 1 diabetes
  2. Type 2 diabetes patients who takes mealtime insulin therapy
  3. Injected sc before meals as an adjunct to insulin therapy to control postprandial hyperglycemia

amylin analog

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37
Q

What drugs can interact with pramlintide?

A

it enhances anticholinergic effects of drugs on the GI tract (ie constipation)

38
Q

What endogenous factors regulate insulin secretion? (3)

A
  1. Glucose and other energy substrates
  2. GPCR-Gs ligands (Beta2-AR agonist and GLP-1 receptor agonist, incretins)
  3. GPCR-Gi ligands (somatostatin and alpha2 -AR agonists)
39
Q

What are the targets of drugs in the regulation of insulin secretion? (3)

A
  1. Resting membrane potential and specifically K-ATP channel
  2. VDCC (L-type Ca2+ channel)
  3. GPCR-Gs/GPCR-Gi-cAMP axis
40
Q

What is Glucagon-like peptide- (GLP-1)?

A

GLP-1 is an Incretin

  1. Synthesized by intestinal L-cells
  2. Promotes: β-cell proliferation, Insulin gene expression, Glucose-dependent insulin secretion
  3. Inhibits glucagon secretion
  4. Also causes satiety, inhibits gastric emptying
  5. Very short half-life (1-2 min) – not an effective drug
41
Q

What are Incretins?

A

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

42
Q

What are the 2 types of incretin mimetics?

A
  1. Long-acting GLP-1 receptor agonists

2. Dipeptidyl peptidase-4 (DPP-4) inhibitors

43
Q

What are Exenatide and Liraglutide?

A

Long-acting GLP-1 receptor agonists insulin secretagogues

do NOT cause hypoglycemia

* Can cause pancreatis*

44
Q

What has a longer half life? Exenatide or Liraglutide?

A

Liraglutide: 11-15 hr half life

Exenatide: 2.4 hr half life

45
Q

What are the clinical uses of GLP-1 receptor agonists (Exenatide and Liraglutide)?

A
  • T2DM diabetic patients who’s diabetes is not adequately controlled
  • The release of GLP-1 is diminished postprandially in type 2 diabetes patients → inadequate glucagon suppression and excessive hepatic glucose output
46
Q

What drug class are

  • Stiagliptin
  • Linagliptin
  • Saxagliptin
  • Alogliptin

(like SaLSA)

A

DPP-4 inhibitor- Gliptins

insulin secretagogues

  • can increase the risk of nasopharyngitis and URI
47
Q

What is MOA of DPP-4 inhibitors (Sitagliptin

• Linagliptin • Saxagliptin • Alogliptin)?

A
  1. DPP-4 is a serine protease that degrades GLP-1 and other incretins
  2. if DPP-4 is inhibited, Increased levels of GLP-1 enhance interactions with a cognate receptor
  3. has similar effects GLP-1 agonists

do NOT cause hypoglycemia (along with GLP-1 agonists)

  • can increase the risk of nasopharyngitis and URI
48
Q

What is the clinical use of DPP-4 inhibitors(Sitagliptin

• Linagliptin • Saxagliptin • Alogliptin) gliptins?

A
  1. Adjunct therapy to diet and exercise in patients with T2DM
  2. mono therapy in combo with metformin and sulfonlylureas, taken orally

do NOT cause hypoglycemia

  • can increase the risk of nasopharyngitis and URI
49
Q

What is Sitagliptin?

A

DPP-4 inhibitor- gliptin
insulin secretagogues

  • can increase the risk of nasopharyngitis and URI
50
Q

What is Linagliptin?

A

DPP-4 inhibitors - gliptin
insulin secretagogues

  • can increase the risk of nasopharyngitis and URI
51
Q

What is Saxagliptin?

A

DPP-4 inhibitor

insulin secretagogues

52
Q

What is Alogliptin?

A

DPP-4 inhibitor

53
Q

What are Chlorporpamide, Tolbutamide, and Tolazamide?

  • amides
A

First generation Sulfonylureas, Potassium (ATP) channel blockers

  • amides is suffix
54
Q

What is Chlorporpamide?

A

First generation Sulfonylureas, Potassium (ATP) channel blockers

  • can cause a disulfiram like rxn (along with some other first generation -amides)
55
Q

What is Tolbutamide?

A

First generation Sulfonylureas, Potassium (ATP) channel blockers

56
Q

What is Tolazamide?

A

First generation Sulfonylureas, Potassium (ATP) channel blockers

57
Q

What are Glipizide, Glyburide, and Glimepiride?

A

Second generation Sulfonylureas, Potassium (ATP) channel blockers

58
Q

What is Glipizide?

A

Second generation Sulfonylureas, Potassium (ATP) channel blockers

59
Q

What is Glyburide?

A

Second generation Sulfonylureas, Potassium (ATP) channel blockers

60
Q

What is Glimepiride?

A

Second generation Sulfonylureas, Potassium (ATP) channel blockers

61
Q

What are Nateglinide and Repaglinide?

A

Non-sulfonylureas, Potassium (ATP) channel blockers

62
Q

What is Nateglinide?

A

Non-sulfonylureas, Potassium (ATP) channel blockers

63
Q

What is Repaglinide?

A

Non-sulfonylureas, Potassium (ATP) channel blockers

64
Q

What is the difference between first and second generation sulfonylureas?

A

First–> lower potency( used in high doses), not used much now

Second–> higher potency (used in low mg doses), fewer adverse effects

65
Q

What is the MOA of Potassium (ATP) channel blocker (insulin secretagogues?

A
  1. binds the sulfonylurea receptor (SUR1)
  2. Blocks potassium current through Kir6.2 inwardly rectifying potassium channel
  3. End result is release of endogenous insulin
66
Q

What is the the clinical use fo sulfonylurea?

A

T2DM as mono therapy or in combo with insulin or other anti-diabetic drugs

67
Q

What are the adverse effects of sulfonylureas?

A
  1. Hypoglycemia
  2. Weight gain (due to increased insulin release)
  3. Secondary failure – patients who respond initially later cease to respond to sulfonylureas and develop unacceptable hyperglycemia
68
Q

What drugs enhance the hypoglycemic effect of sulfonylureas and how?

A

– Displacing from binding with plasma proteins:

  1. sulfonamides
  2. clofibrate
  3. salicylates
  4. other NSAIDs

– Ethanol

– Inhibiting CYP enzymes:

  1. azole antifungals
  2. gemfibrozil
  3. cimetidine, etc.
69
Q

What drugs decrease the glucose lowering effects of sulfonylureas and how?

A

– Inhibiting insulin secretion:

  1. beta-blockers
  2. CCBs

– Inducing hepatic CYP enzymes:

  1. phenytoin
  2. griseofulvin
  3. rifampin
70
Q

What is the MOA of Meglitinides (Repaglinide and Nateglinide)?

A

K(ATP) channel inhibition (similar to sulfonylureas)

  • Bind ATP dependent K+ on Beta cells to increase release of endogenous insulin
  • Meglitinides (and sulfonylureas) increase the release of insulin and C peptides
71
Q

What is the clinical use of Meglitinides (Repaglinide and Nateglinide)?

A
  1. Control of postprandial hyperglycemia in patients with type 2 diabetes
  2. Taken orally before the meal
  3. Can be used either alone (to control isolated postprandial hyperglycemia) or in combination with other antidiabetic drugs
72
Q

What are the adverse effects of Meglitinides (Repaglinide and Nateglinide)?

A

– Hypoglycemia
– Weight gain
– Secondary failure

73
Q

What is the MOA of Metformin?

A

Activation of AMP-activated protein kinase

74
Q

What type of drug is Metformin?

A

BIGUANIDES

75
Q

What is the clinical use of metformin?

A
  • The most commonly used oral agent to treat type 2 diabetes
  • generally accepted as the first-line treatment for this condition
76
Q

What are the Advantages in using Metformin?(6)

A
  1. Superior or equivalent glucose-lowering efficacy compared to other oral medications
  2. Does not cause hypoglycemia
  3. Does not cause weight gain
  4. Taken orally
  5. Can be used either alone or in combination with other oral agents
  6. In clinical trials decreased the risk of both macro- and microvascular complications in diabetic patients
77
Q

What are the adverse effects of Metformin?

A
  1. Most common: GI complications – anorexia, vomiting, nausea, diarrhea, abdominal discomfort
  2. Lactic acidosis, especially under conditions of hypoxia, renal and hepatic insufficiency
78
Q

What are the contraindications of Metformin?

A

Contraindicated in conditions that predispose tissue hypoxia

  • HF,
  • COPD
  • renal failure
  • Chronic alcoholism
  • cirrhosis
79
Q

What are pioglitazone and rosiglitazones?

A

Thiazolidinediones

80
Q

What is the MOA of Thiazolidinediones (pioglitazone and rosiglitazone)?

A

– Ligands of peroxisome proliferator-activated receptor-gamma (PPARγ)

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

81
Q

What are the effects of Thiazolidinediones (pioglitazone and rosiglitazone)?

A

↑Glut4 in skeletal muscle

↑Glut4 in adipocytes

↑IRS1, IRS2, PI3K

↓PEPCK

↓NF-κB, AP-1

82
Q

What is unique about Thiazolindione metabolism?

A
  • Onset is delayed – full effect develops after 1 to 3 months

• Effects persist after drugs are eliminated for weeks-months

Metabolized by the liver
• Half-life is reduced by CYP-inducing drugs (rifampin)
• Half-life is prolonged by CYP-inhibiting drugs (gemfibrosil)
– Safe to administer to patients with renal failure

83
Q

What is the clinical use of Thiazolindinediones?

A

Type 2 diabetes, alone or in combination with other antidiabetic drugs

– Shown to delay progression from prediabetes to type 2 diabetes

– Euglycemic drugs (no hypoglycemia when used alone)

84
Q

What are the adverse effects of Thiazolindinediones?

A
  • Increase vascular permeability (mechanism is currently unknown)
  • Increase expression of ENaC (epithelial Na+ channel) – increased sodium and water reabsorption in the collecting duct

– Exacerbation of heart failure
• Due to increased water retention
• No direct effect on cardiac contractile function • Contraindicated in patients with congestive HF

– Osteoporosis – bone fractures (especially in postmenopausal women)
• Direct MSCs to adipocyte differentiation
• Suppress differentiation of MSCs into osteoblasts

85
Q

What are Canagliflozin, Dapagliflozin, and Empagliflozin?

A

SODIUM-GLUCOSE CO-TRANSPORTER 2 INHIBITORS (SGLT2 INHIBITORS OR GLIFLOZINS)

SGLT2 inhibitors

86
Q

What is MOA of SODIUM-GLUCOSE CO-TRANSPORTER 2 INHIBITORS (SGLT2 INHIBITORS OR GLIFLOZINS)?

A

inhibit SGLT2 in the proximal tubule to increase glucose excretion and to reduce hyperglycemia

87
Q

What is the clinical use of sodium-glucose Co-Transporter 2 inhibitors?

A

– In adults with type 2 diabetes in combination with other agents

– Taken orally before the first meal once a day

– In patients with hypovolemia, this condition should be corrected before the start of therapy

88
Q

War are the adverse effects of sodium-glucose Co-Transporter 2 inhibitors?

A

Orthostatic hypotension, dizziness, syncope

89
Q

What are Acarbose and Miglitol?

A

α-Glycosidase inhibitors

  • Reduce monosaccharide absorption
  • lower postprandial hyperglycemia–> insulin sparing
90
Q

What is adverse effect of α-Glycosidase inhibitors ( Acarbose and Miglitol?)

A

– Most common: malabsorption, flatulence, diarrhea, and abdominal bloating

– Hypoglycemia has been described when combined with insulin or insulin secretagogues

RE Pharm (3 decks)

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