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Pharmacology Test 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Primary forms of Diabetes

A

Type 1

Type 2

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2
Q

Type 1 Diabetes

A
  • selective B-cell destruction, severe or absolute insulin deficiency
  • juvenile onset
  • – 1A: autoimmune
  • – 1B: non-autoimmune
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3
Q

Type 2

A
  • late onset
  • tissue resistance to insulin
  • usually adult onset
  • obesity is common/predisposing factor
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4
Q

Type 3

A

Other

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5
Q

Type 4

A

Gestational

- affecting 4% of pregnant women

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6
Q

Glucose concentration cutoff

A

Above 5.7 => diabetes

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7
Q

Regulation of Blood Glucose Concentration

A
  • negative feedback
  • food triggers insulin release
  • stimulates absorption of glucose
  • decrease in blood [glucose]
  • decrease blood [glucose] => decreased insulin levels
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8
Q

Regulation of Blood Glucose Concentration

A
  • liver
  • muscle
  • adipose
  • pancreatic B cells
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9
Q

Insulin Receptor

A
  • glucose transporter translocation to membrane
  • glucose uptake increases
  • glycogen synthase activity increases (glycogen formation increases)
  • increase in lipogenesis and protein synthesis
  • enhance DNA synthesis and cell growth and division
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10
Q

Glucose stimulates

A

insulin secretion

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11
Q

Diabetes Complications

A

prolonged exposure of tissues to increased concentrations of glucose => development and complications of diabetes

  • Glycation of protein
  • glycosylated hemoglobin A1c

** formation of sorbitol => increased glucose uptake, aldose reductase converts glucose to sorbitol in neurons, increased osmotic effect, cell death **

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12
Q

Formation of sorbitol

A
  • increased glucose uptake
  • aldose reductase converts glucose to sorbitol in neurons
  • increased osmotic effect
  • cell death
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13
Q

Peripheral nerve complications

diabetes

A
  • selling -> neuropathies
  • aldose reductase converts glucose -> sorbitol
  • amputation
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14
Q

GI system complications

diabetes

A
  • decreased autonomic nerve activity
  • constipation
  • gastric stasis
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15
Q

Kidney, capillary membrane complications

diabetes

A
  • thickening, scarring, coarsening
  • worsened by hypertension
  • accelerates atherosclerosis
  • protein glycation and cross-linking => irreversible protein accumulation

RENAL FAILURE

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16
Q

Retina complications

diabetes

A
  • blindness
  • protein glycation
  • damaged capillary wall -> proliferation new capillaries
  • blindness
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17
Q

Skin complications

diabetes

A
  • slowed mucopolysaccharide turnover

- impaired wound healing

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18
Q

heart and cardiovascular system complications

diabetes

A

death

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19
Q

Controlling blood glucose levels means

A

delaying complications

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20
Q

Treatment of diabetes

A
  • no cure
  • lifetime control
  • – blood glucose levels - glycemic control
  • prevent or delay development of diabetic complications
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21
Q

Type I Diabetes

A
  • loss of insulin-producing B cells
  • DEFICIENCY OF INSULIN
  • B cell loss due to autoimmune attack
  • juvenile diabetes
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22
Q

Treatment of Type I Diabetes

A

insulin supplement

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23
Q

Pharmacotherapy with Insulin

A
  • short acting/long acting

- used in combination to achieve insulin levels which mimic physiological fluctuations

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24
Q

Regular Insulin

A
  • short acting
  • SC Prep
  • IV Prep
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25
Q

S. C. Prep

  • effect timing
  • peak
  • duration
A
  • short acting insulin
  • injection
  • effects appear within 30 minutes
  • peak at 2-3 hours
  • lasts 5-8 hours
  • ZN2+
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26
Q

I. V. Prep

A
  • diluted
  • phosphate buffered
  • especially useful for crisis situations
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27
Q

Ultra-short acting (rapid-acting) insulin analogues

A
  • mutated molecule; changes pharmacokinetic properties, but NOT activity
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28
Q

Lispro

A
  • Ultra-short acting (rapid-acting) insulin analogues
  • human insulin analog
  • biologic effects ~ regular human insulin
  • aggregates less
  • absorbed more rapidly
  • shorter duration
29
Q

Aspart

A
  • Ultra-short acting (rapid-acting) insulin analogues
  • human insulin analog
  • properties similar to Lispro
  • biologic effects ~ regular human insulin
  • aggregates less
  • absorbed more rapidly
  • shorter duration
30
Q

Flulisine

A
  • Ultra-short acting (rapid-acting) insulin analogues
  • human insulin analog
  • similar to others
31
Q

Basal Insulin Analogues

A
  • long acting
  • take very long time to release
  • superior to traditional long-lasting insulins; more expensive
32
Q

Glargine

A

Basal Insulin Analogues

- human insulin analog

33
Q

Detemis

A

Basal Insulin Analogues

- human insulin analog

34
Q

Human Insulin Analogs

A
  • amino acid sequence changed with altered pharmacokinetic properties
  • no change in binding and activating insulin receptor
35
Q

Insulin Delivery Systems

A
  • syringes/needles
  • portable pen-sized injectors
  • continuous subcutaneous insulin infusion pumps
36
Q

Insulin Regimens

A
  • basal insulin + pre-meal short acting insulin
  • NPH insulin + regular insulin
  • s.c. insulin pump
37
Q

Type 2 Diabetes

  • cause
  • intervention
  • goal
A

Cause

  • tissue resistance to insulin action
  • a RELATIVE deficiency in insulin secretion
  • aging and obesity are a predisposing factor

Intervention

  • dietary control + weight reduction
  • oral or injectable hypoglycemia agents
  • insuling
  • – right amount of insulin at the right time for the right situation

Goal

  • control blood glucose concentration
  • delay development of complications
38
Q

Metformin

A
  • first line TYPE 2 diabetes drug
  • decrease liver glucose release
  • increase GLP-1 release
  • highly effective in reducing A1C, without causing hypoglycemia
  • not metabolized by liver; excreted unchanged
  • t1/2 1.5-3 hours
    __________________________________________
    ***- target liver
  • decrease hepatic glucose output
  • decrease fasting glucose***
39
Q

Metformin Mechanism of Action

A
  • main target organ: liver: decrease hepatic glucose output, decrease fasting glucose
  • also increase GLP-1 secretion
  • anti-hyperglycemia, not hypoglycemic: lowers glucose to “euglycemia” levels
  • does not increase body weight and may help obese pts. lose weight!
40
Q

Metformin Metabolism & Excretion

A
  • t1/2 1.5-3 hours
  • is NOT metabolized by liver
  • excreted unchanged
41
Q

Insulin Secretogogues

A
  • sulfonylureas
  • sensitize B cells
  • target ATP-sensitive K+ channel action depends on a functional B-cell
  • binds K & lower threshold => less ATP needed to release insulin
  • increase ATP in cell -> close K+ channel (depolarization) -> Ca2+ floods in -> insulin release
42
Q

The Sulfonylureas

A
  • 2nd generation agents
  • increased potency (100X)
  • less required
  • less adverse effects
43
Q

glyburide

A

sulfonylurea

44
Q

glipizide

A

sulfonylurea

45
Q

glimepiride

A

sulfonylurea

46
Q

Sulfonylurea mechanism

A
  • stimulation of insulin release from B cells

- high affinity binding to a B-cell receptor associated with an ATP-sensitive, inward rectifier K+ channel

47
Q

Thiazolidinediones

“glitazones”

A
  • takes a couple months to see effect
48
Q

acarbose

A

a-flucosidase inhibitors

49
Q

a-flucosidase inhibitors

A
  • competitive inhibitors of intestinal a-glucosidases, enzymes that digest dietary complex starches, oligosaccharides, and disaccharides to absorbable monosaccharides
  • upper intestinal digestion of starch + disaccharides decrease
  • decrease in digestion
50
Q

Incretin GLP-1-based therapies

A

stimulate insulin secretion after a meal

51
Q

GLP-1

A
  • an incretin
  • stimulates glucose-dependent insulin secretion
  • inhibits glucagon release
  • delays gastric emptying
  • reduces food intake
  • normalizes fasting and postprandial insulin secretion
52
Q

incretin

A

GI hormone that is released after meals and stimulate insulin secretion

53
Q

GLP-1 rapidly inactivated by

A
  • DPP-4
54
Q

GLP-1 t1/2

A

very short

55
Q

DPP-4

Dipeptidyl peptidase IV

A
  • cleaves GLP1

- – why GLP1 has such a short t1/2

56
Q

2 types GLP-1 based therapeutics

A
  • injectable DPP-4 resistant peptide agonists of the GLP-1 receptor
  • small molecule inhibitors of DPP-4
57
Q

Exenatide

A

DPP-4 resistant peptide agonist of GLP-1 receptor

58
Q

Sitagliptin

A
  • small molecule inhibitors of DPP-4
  • prolong GLP1 t1/2
  • increase GLP => increase insulin
59
Q

Kidney SGLT2

A
  • ONLY type 2

- inhibit gliflozins

60
Q

Major Therapeutic Categories

Oral

A
  • Metformin
  • Insulin Secretogogues
  • Kidney SGLT2 inhibitors
  • DPP-4 inhibitors
  • Thiazolidinesdiones
  • a-glucosidase inhibitors
61
Q

Metformin

A
  • major target liver, decreasing hepatic glucose output and lower fasting blood glucose levels
  • a biguanide
62
Q

Insulin Secretogogues

A
  • target pancreatic B-cells, potentiating insulin secretion

- sulfonylureas and meglitinides

63
Q

Gliflozins

A

Kidney SGLT2

64
Q

DPP-4 inhibitors

A

increase GLP-1 and GIP

65
Q

Thiazolidinediones

A
  • target adipose, as well as muscle and liver, increasing peripheral insulin sensitivity
66
Q

a-glucosidase inhibitors

A

target intestinal a-glucosidases, reducing glucose absorption

67
Q

Major Therapeutic Categories

Injectables

A
  • GLP-1 agonists
  • Amylin agonists
  • Insulin
68
Q

GLP-1 Agonists

A
  • potentiate insulin secretion
  • suppress glucagon secretion
  • slow gastric motility
69
Q

Amylin agonists

A
  • slow gastric emptying

- inhibit glucagon productions

Pharmacology Test 2 (8 decks)

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