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pharmocology > diabetic drugs > Flashcards

diabetic drugs Flashcards

1
Q

The Pancreas

• Can be found just “tucked in”

A

the angle formed by the gastric pylorus and the proximal duodenum

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2
Q

The Pancreas

• You’ve already learned it has two functions:

A

1) Exocrine (various digestive enzymes)

2) Endocrine

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3
Q

The Endocrine Pancreas

A

Produces insulin (signalling a “fed” state), glucagon (signalling a “hungry” state), gastrin, somatostatin, and many others. releases into blood stream

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4
Q

Beta cells

A

secrete insulin which causes BG to decrease (after all, you’re in the fed state and need to stash that
energy)

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5
Q

alpha cells

A

secrete glucagon which causes BG to

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6
Q

delta cells

A

secrete somatostatin which regulates a LOT of things (and gets
very, very complicated!)

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7
Q

The Exocrine Pancreas

A 
Releases bicarb (why?) reverses bicarb so digestive zymogens can work and digestive zymogens to break down fats and proteins
• All goes awry with pancreatitis
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8
Q

) Diabetes insipidus

A

Critter doesn’t produce or kidneys don’t respond toVasopressin (Antidiuretic Hormone/ADH)

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9
Q

diabetes mellitus type 1

A

Insulin-Dependent DM (IDDM)”

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10
Q

DM type 2

A

Non-Insulin-Dependent DM (NIDDM) Broadly, Type 1 DM is an absolute insulin deficiency and Type 2 DM is a relative deficiency of insulin

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11
Q

DM type 3

A

Other

• Due to side effects of drugs, toxins, viral infections, genetic predispositions, etc. Variable in course & treatment

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12
Q

DM type 4

A

Gestational
• Women may develop extreme insulin resistance during their third trimesters of pregnancy (same time they might be prone to blowing out mitral valves, eh?) as a result of hormonal changes

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13
Q

Type 1 DM

• These critters must receive insulin or suffer from the four “classic” symptoms of hyperglycemia:

A

Polyphagia -Polydipsia -Polyuria -Polyweightloss(?)

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14
Q

Type II DM

• These critters produce variable

A

amounts of insulin and exhibit insulin resistance.

»These critters typically require increasing doses of insulin and combination therapy with other antihyperglycemics

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15
Q

uncontrolled Type 4 DM can lead to

A

xtremely large babies, dystocia, and neonatal hypoglycemia

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16
Q

why are plasma insulin levels are not an accurate measure of insulin production

A

nsulin is removed from circulation so rapidly (3-5 minute half-life). c protein measurement better guide

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17
Q

C-Protein

A

NOT to be confused with Protein C or C- reactive protein!

• A 31 amino acid peptide used to differentiate Type 1 DM from Type 2 DM

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18
Q

Half-life of C-Protein is

A

~30 minutes

– Therefore ~5X as much in the blood stream as insulin

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19
Q

insulin is produced by

A

β-cells in the pancreas in response (generally) to glucose (the archetypical “fed state”)

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20
Q

Insulin’s main effect target tissues are

A

liver, fat, and muscle

• Insulin exhibits anabolic effects on these target tissues

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21
Q

Insulin is increasingly being used by perfusionists for

A

hyperkalemia therapy (what’s this? what’s “normalkalemia?), often in conjunction with glucose to “drive” potassium intracellularly

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22
Q

hat else can you do to lower potassium levels?

A

?

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23
Q

…perfusionists have started to seek much “finer” control of glucose levels on bypass, so

A

insulin drip and anti-hyperglycemic protocols have become much more common.

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24
Q

Rapid onset/short-acting insulin

A

Regular insulin (Humulin R, Novolin R) -Insulin aspart (Novolog) -Insulin glulisine (Apidra) -Insulin lispro (Humalog). Given IV or subcutaneously (SQ)

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25
Q

regular insulin

A

(Humulin R, Novolin R) Rapid onset/short-acting insulin

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26
Q

insulin aspart

A

(novolog) Rapid onset/short-acting insulin

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27
Q

insulin glulisine

A

(apidra) Rapid onset/short-acting insulin

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28
Q

insulin lispro

A

(humalog) Rapid onset/short-acting insulin

29
Q

-Neutral Protamine Hagedorn (NPH) insulin

A

(Humulin N, Novolin N) *Only given SQ. its only intermediate lasting insulin

30
Q

Long acting insulins

A

Insulin glargine (Lantus) -Insulin detemir (Levemir)

  • Both have fatty-acid side-chain attachments that cause them to bind albumin for longer action.
  • Give only SQ
  • Do NOT mix with other types of insulin!
31
Q

Insulin glargine

A

(Lantus) Long acting insulins

32
Q

Insulin detemir

A

(Levemir) Long acting insulins

33
Q

Various mixtures of

A

compatible insulin also exist.

• The goal is to minimize hyper- and hypoglycemia

34
Q

Why “Fine” Glucose Control is Important

A

decreases retinopathy and nephropathy

35
Q

Fine” Glucose Control Measurement

A

TheADArecommendsdiabetics’blood glucose (BG) maintain a mean of 154 mg/ml.

36
Q

Long-term BG measurement is via

A

Glycated (glycosylated) Hb (HbA1c)

37
Q

*Normal HbA1C is

A

<7.0%

38
Q

Pramlintide

A

(Symlin) ia an amylin analog. B cells make it

39
Q

Amylin is a

A

polypeptide released by the pancreas in conjunction with insulin

40
Q

amylin works with insulin by

A

to moderate physiologic glucose levels by slowing gastric emptying and digestion (why would this be a good thing…remember, insulin is the hormone signalling a “fed” state)

41
Q

By slowing digestion Pramlintide

A

spreads out” glucose absorption over a longer period.
• Given SQ at meals. • Also causes post-
prandial satiety

42
Q

Incretin Mimetics

-

A
  • Exenatide (Byetta): SHORT ACTING -Liraglutide (Victoza): LONG ACTING. Both are proteins that are given SQ prior to eating
  • Side effects are mainly GI
43
Q

Exenatide

A

(Byetta): SHORT ACTING Incretin Mimetics

44
Q

Liraglutide

A

(Victoza): LONG ACTING Incretin Mimetics

45
Q

*Incretins are hormones

A

released by the GI tract post-prandially that stimulate the pancreas to release insulin, slow gastric emptying, decrease glucagon release, and encourage β-cell growth

46
Q

Oral Insulin “Adjuncts”

• Often used as part of

A

progressive combination

therapy” for Type 2 DM.

47
Q

Insulin Secretagogues

A

Increase β-cells production of insulin (so critter must still have functioning pancreas), lower hepatic glucose production, and increase peripheral insulin sensitivity.

48
Q

-Glyburide

A

(Diabeta, Micronase) Insulin Secretagogues Sulfonylureas

49
Q

glimepiride

A

(Amaryl) Insulin SecretagoguesSulfonylureas

50
Q

glipizide

A

(Glucotrol) Insulin Secretagogues Sulfonylureas

51
Q

-Nateglinide

A

(Starlix) Insulin Secretagogues glinide

52
Q

Repaglinide

A

(Prandin) Insulin Secretagogues glinide

53
Q

Insulin Sensitizers

A

Increase peripheral cellular sensitivity to insulin without increasing insulin secretion (why might this be a good thing?)

54
Q

metformin

A

(Glucophage) insulin sensitizer Biguanides

55
Q

Pioglitazone

A

(Actos) insulin sensitizer Thiazolidinediones

56
Q

-Rosiglitazone

A

(Avandia) insulin sensitizer Thiazolidinediones

57
Q

Biguanides

A

Prevents hepatic gluconeogenesis (huh?)
***This is very important because hepatic glucose production is the main source of excessive glucose in Type-2 DM! Often used in combination with insulin or other oral antiglycemics
• Diarrhea is a very common side-effect

58
Q

Thiazolidinediones

A

Increase intracellular receptors in skeletal muscle, liver, and adipose tissue to become more sensitive to endogenous insulin.
• Side effects include weight gain, liver damage, and increased CV risks (a bad thing) & others

59
Q

α-Glucosidase Inhibitors

A
  • Acarbose (Precose) -Miglitol (Glyset)
  • Work by reversibly inhibiting an enzyme in the small intestines that helps digest polysaccharides into simple sugars.
  • This delays complex sugar digestion which “spreads out” the post-prandial blood glucose spike. *Don’t cause hypoglycemia by themselves, but will contribute significantly in combination RX.
60
Q

Acarbose

A

(precose) α-Glucosidase Inhibitors

61
Q

miglitol

A

(glyset) α-Glucosidase Inhibitors

62
Q

Dipeptidyl Peptidase-IV Inhibitors

A

Saxagliptin onglyza -Sitagliptin (Januvia)*Work at the cellular level to increase post- prandial insulin release while inhibiting glucagon (insulin’s physiologic antagonist) release.

63
Q

Saxagliptin

A

Onglyza). Dipeptidyl Peptidase-IV Inhibitors

64
Q

-Sitagliptin

A

Januvia) Dipeptidyl Peptidase-IV Inhibitors

65
Q

SGLT2 is a

A

low affinity, high capacity transport mechanism in the proximal tubule. It’s designed to “capture” glucose lost in renal filtration

66
Q

Sodium Glucose Co-Transporter Inhibitors (SGLT Inhibitors)

• Glucose is therefore

A

freely “lost” into the urine.

67
Q

Canagliflozin

A

(Inkovana) Sodium Glucose Co-Transporter Inhibitors (SGLT Inhibitors)

68
Q

Dapagliflozin

A

(Farxiga) was almost approved for use in the U.S. (and is still used extensively in Europe) but it was found to have one small side- effect (besides nasty intractable urinary tract yeast infections. bladder cancer but got approved A 6-fold increase in bladder cancer.

pharmocology (20 decks)

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