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pharmacology 4810 > Insulin Preps MT2 > Flashcards

Insulin Preps MT2 Flashcards

1
Q

this is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, action or both

A

diabetes

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2
Q

how are glucose utilization, glucose production and insulin secretion affected in DM

A

glucose utilization: decreased
glucose production: increased
insulin secretion: decreased

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3
Q

normally, blood glucose levels are tightly controlled by _______ which is a hormone produced by the pancreas

A

insulin

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4
Q

what are the three main symptoms of diabetes

A

polydipsia - excessive thirst
polyphagia - increased appetite
polyuria - excessive passing of urine

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5
Q

type I or type II DM?
onset occurs usually < 20 y/o

A

type I

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6
Q

type I or type II DM?
obesity is usually present

A

type II

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7
Q

type I or type II DM?
onset occurs usually > 30 y/o

A

type II

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8
Q

type I or type II DM?
normal or increased blood insulin

A

type II

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9
Q

type I or type II DM?
decreased blood insulin

A

type I

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10
Q

type I or type II DM?
anti-islet cell antibodies are present

A

type I

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11
Q

type I or type II DM?
ketoacidosis is common

A

type I

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12
Q

type I or type II DM?
50% concordance in twins

A

type I

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13
Q

type I or type II DM?
60-80% concordance in twins

A

type II

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14
Q

type I or type II DM?
no HLA association

A

type II

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15
Q

type I or type II DM?
HLA-D linked

A

type I

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16
Q

type I or type II DM?
severe insulin deficiency

A

type I

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17
Q

type I or type II DM?
insulin resistance is present

A

type II

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18
Q

type I or type II DM?
autoimmune, immunopathologic mechanisms present

A

type I

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19
Q

type I or type II DM?
no insulitis present

A

type II

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20
Q

type I or type II DM?
marked atrophy and fibrosis

A

type I

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21
Q

type I or type II DM?
focal atrophy and amyloid deposits (amyloid gets secreted alongside insulin and if have this type of DM the amyloid gets deposited)

A

type II

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22
Q

type I or type II DM?
severe beta-cell depletion

A

type I

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23
Q

type I or type II DM?
mild beta-cell depletion

A

type II

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24
Q

what are some of the organs/systems that complications may occur in DM

A
  • cardiovascular
  • eyes
  • kidneys
  • nervous systems
  • pancreas
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25
Q

what is used to diagnose diabetes

A
  • fasting plasma glucose (above 7 mol/L)
  • plasma glucose (above 11.1 mol/L)
  • hemoglobin A1c (above 6.5%)
  • symptoms of DM
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26
Q

true or false: type 1 DM is reversible

A

false

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27
Q

true or false: type 2 DM is reversible

A

true

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28
Q

true or false: gestational DM is reversible

A

true

29
Q

blood glucose levels tend to be higher in untreated ____1____ than untreated ___2____ because _____3____ subjects retain some insulin action

A

1 - type 1
2 - type 2
3 - type 2

30
Q

this is stored in the liver in the form of glycogen

A

glucose

31
Q

its effect is to lower blood glucose levels. it is activated during the fed state, where blood glucose levels are high. low levels release adipocytes from inhibition

A

insulin

32
Q

this peptide increases glucose levels. hepatocytes have receptors for this peptide which convert the glycogen polymer to individual glucose molecules to be released into the blood. when glucose stores are depleted, this peptide induces glycogenolysis by the liver and kidney

A

glucagon

33
Q

this is stored within granules in the beta-cells of the pancreas. the half life is 3-5 mins

A

endogenous insulin

34
Q

two organs are responsible for removing insulin from circulation. these organs are

A
  • liver
  • kidney
35
Q

free insulin binds to insulin receptors primarily on what organs

A

liver, muscle and adipose tissue

36
Q

what type of receptors are insulin receptors?

A

tyrosine kinase
- alpha subunit is the binding domain
- beta subunit is the ATP-binding and tyrosine kinase domains

37
Q

only ___% of insulin receptors need to be occupied to produce the maximum effect

A

10

38
Q

when the activated insulin receptor phosphorylates, it becomes an insulin receptor substrate. rapid effects are mediated by this pathway

A

PI3K

39
Q

when the activated insulin receptor phosphorylates, it becomes an insulin receptor substrate. long term effects are mediated by this pathway

A

MAP kinase

40
Q

this GLUT transporter is found in all tissues, especially red cells and the brain.
function: basal glucose uptake & transport across the BBB

A

GLUT1

41
Q

this GLUT transporter is found in the beta-cells of the pancreas; liver, kidney and gut.
function: regulation of insulin release & glucose homeostasis

A

GLUT2

42
Q

this GLUT transporter is found in the brain, kidney, placenta and other tissues
function: uptake into neurone and other tissues

A

GLUT3

43
Q

this GLUT transporter is found in the muscle and adipose tissue.
function: insulin-mediated uptake of glucose

A

GLUT4

44
Q

this GLUT transporter is found in the gut and kidney
function: absorption of fructose

A

GLUT5

45
Q

what are the different ways insulin preparations differ by?

A
  • source (human or animal species from which they are derived)
  • purity
  • concentration
  • solubility
  • time of onset and duration of action
46
Q

these insulin preparations are dispensed as clear solutions at a neutral pH. they also have small amounts of zinc to increase shelf-life.

A

ultra short acting and short acting insulins

47
Q

these insulin preparations are cloudy and have been modified in some way to permit slower onset and longer duration.

A

intermediate and long acting insulins

48
Q

what are some adverse effects of insulin

A
  • hypoglycaemia
  • loss of fatty tissue at site of injections (rotate!)
  • insulin allergy (rare)
  • insulin resistance (very rare)
49
Q

examples include Insulin Lispro, Insulin Aspart and Insulin Glulisine

A

rapid acting human insulin analogs

50
Q

examples include regular insulin

A

short acting insulin

51
Q

examples include NPH insulin

A

intermediate acting insulin

52
Q

examples include insulin glargine and insulin detemir

A

long acting human insulin analogs

53
Q

what is the onset of action, peak and effective duration of very rapid acting insulin (e.g. Aspart, Glulisine and Lispro)

A

onset: <0.25, peak is 0.5-1.5 hr and may last for 3-4 hrs

54
Q

what is the onset of action, peak and effective duration of short acting (regular) insulin

A

onset 0.5-1 hr, peak is 2-3 hrs and may last for 4-6 hrs

55
Q

what is the onset of action, peak and effective duration of long acting insulin (e.g. detemir, glargine, degludec and NPH - intermediate)

A

onset: 1-4 hrs, peak = relatively constant and may last for 10-42 hrs, depending on specific insulin

56
Q

what is the onset of action, peak and effective duration of combination insulins (long acting and short acting)

A

onset: 0.25-1hr, peak is 1.5 hr and may last for 10-16 hrs

57
Q

what is the FIRST LINE treatment of type II DM

A

lifestyle changes such as diet, weigh loss, exercise, education.

58
Q

what pharmaceutical agents may be used to treat type II DM

A

oral hypoglycemics such as sulphonylureas, biguanides, thiazolidinediones, meglitinides and alpha-glucosidase inhibitors (sometimes insulin)

59
Q

this type of oral hypoglycemic are derived from sulfonic acid and urea. examples include gliclizide, tolbutamide, glyburide, etc.

A

sulphonylureas and secretagogues

60
Q

what are some side effects of sulphonylureas and secretagogues

A

hypoglycaemia
weight gain or anorexia
nausea, heartburn
weakness or numbness of the extremities

61
Q

what is the MOA of sulphonylureas and secretagogues

A

act similar to glucose as they inhibit the ATP sensitive K+ channel, but they bind to the SUR portion. this depolarizes the channel and allows influx of Ca++ which stimulates the release of insulin

62
Q

these oral hypoglycemic enhances secretion of insulin similar to that as sulfonylureas. it has a rapid onset of action and short duration. is generally taken before a meal because if a meal is skipped or delayed it can cause hypoglycemia

A

meglitinides (nateglinide and repaglinide)

63
Q

this oral hypoglycemic agent decreases hepatic glucose production

A

biguanides (metformin)

64
Q

what is the MOA of biguanides (metformin)

A

blocks gluconeogenesis in the liver. increases insulin sensitivity in the muscle and fat by sensitizing the insulin receptors. promotes glucose uptake by skeletal muscle.

65
Q

these drugs are good agents for restoring glucose into normal or non-diabetic range without causing hypoglycemia

A

thizolidinediones (e.g. pioglitazone)

66
Q

what is the MOA of thiazolidinediones

A

agonists of PPAR-gamma. increases the sensitivity of tissues (muscle and adipose) to insulin. reduces insulin resistance

67
Q

what are some side effects of thiazolidinediones

A

weight gain, edema, GI, h/a, increased respiratory infections

68
Q

what is the MOA of alpha-glucosidase inhibitors (acarbose)

A

competitive inhibitor of intestinal alpha-glucosidase (enzyme that breaks down disaccharides). delays absorption of carbohydrates from the gut. reduces postprandial glucose rise

69
Q

what are some side effects of alpha-glucosidase inhibitors

A

GI!!! may wanna stay away from this drug

pharmacology 4810 (12 decks)

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