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Pharm Final > Topic 18 Diabetics > Flashcards

Topic 18 Diabetics Flashcards

1
Q

The Endocrine Pancreas produces what ?

A

Produces insulin (signalling a “fed” state), glucagon (signalling a “hungry” state), gastrin, somatostatin, and many others

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2
Q

Beta cells secrete

The Endocrine Pancreas

A

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

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3
Q

Alpha cells secrete

The Endocrine Pancreas

A

glucagon which causes BldGlucose to INCREASE

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4
Q

Delta cells secrete

The Endocrine Pancreas

A

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

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5
Q

What goes awry with pancreatitis?

A

The Exocrine Pancreas

•Releases bicarb and digestive zymogens to break down fats and proteins

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6
Q

Diabetes insipidus- Critter doesn’t produce or kidneys

A

don’t respond to Vasopressin (Antidiuretic Hormone/ADH)

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7
Q

Type 1 DM is an absolute what?

A

Broadly, Type 1 DM is an absolute insulin deficiency and Type 2 DM is a relative deficiency of insulin

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8
Q

All DM is characterized as what?

A

as an absolute or relative deficiency of insulin

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9
Q

Type 1 DM:

A

“Insulin-Dependent DM (IDDM)”

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10
Q

Type 2 DM:

A

“Non-Insulin-Dependent DM (NIDDM)”

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11
Q

Classic symptoms of hyperglycemia (4)

A
  • Polyphagia
  • Polydipsia
  • Polyuria
  • weightloss
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12
Q

Women may develop extreme insulin

resistance – what kind of diabetes is this???

A

DM TYPE 4
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
•Controlled with insulin: uncontrolled Type 4 DM can lead to extremely large babies, dystocia, and neonatal hypoglycemia

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13
Q

Insulin is a small polypeptide consisting

of two chains connected by what?

A

a disulfide bond

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14
Q

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

A

C-Protein

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15
Q

Insulin is produced by ____ in the _____ in response (generally) to glucose (the archetypical ______)

A

β-cells in the pancreas

glucose (the archetypical “fed state”)

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16
Q

Insulin exhibits _____ on these target tissues

A

anabolic effects

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17
Q

What increasingly being used by perfusionists for hyperkalemia therapy ?

A

Insulin

often in conjunction with glucose to
“drive” potassium intracellularly

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18
Q

Regular insulin

A

Humulin R, Novolin R

Rapid onset/short-acting Insulin
Given IV or subcutaneously (SQ)

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19
Q

Insulin aspart

A

Novolog

Rapid onset/short-acting Insulin
Given IV or subcutaneously (SQ)

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20
Q

Insulin glulisine

A

Apidra

Rapid onset/short-acting Insulin
Given IV or subcutaneously (SQ)

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21
Q

Insulin lispro

A

Humalog

Rapid onset/short-acting Insulin
Given IV or subcutaneously (SQ)

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22
Q

Neutral Protamine Hagedorn (NPH) insulin

A

Humulin N, Novolin N

Intermediate onset/intermediate acting Insulin
Only given SQ

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23
Q

Insulin glargine

A

Lantus

Long acting insulins
Do NOT mix with other types of insulin
Give only SQ

24
Q

Insulin detemir

A

Levemir

Long acting insulins
Do NOT mix with other types of insulin
Give only SQ

25
Q

Long-term BG measurement is via what?

A

Glycated (glycosylated) Hb (HbA1c)

26
Q

Pramlintide

A

Symlin

Injectable Antihyperglycemics
An “Amylin” analogue

27
Q

Amylin

A

is a polypeptide released by the pancreas in conjunction with insulin
works with insulin to moderate physiologic glucose levels by slowing gastric emptying and digestion

28
Q

Exenatide

A

(Byetta) : SHORT ACTING

Incretin Mimetics

29
Q

Liraglutide

A

(Victoza) : LONG ACTING

Incretin Mimetics

30
Q

Incretins are hormones released by what and that stimulate the pancreas to release what?

A

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

31
Q

Incretins side affects

[Exenatide and liraglutide]

A

Side effects are mainly GI

32
Q

Incretins both are given how?

[Exenatide and liraglutide]

A

Both are proteins that are given SQ prior

to eating

33
Q

Oral Insulin adjuncts (5)

A
  • Insulin Secretagogues
  • Insulin Sensitizers
  • α-Glucosidase Inhibitors
  • Dipeptidyl Peptidase-IV Inhibitors
  • Sodium Glucose Co-Transporter Inhibitors (SGLT Inhibitors)
34
Q

Oral Insulin adjuncts often used as port of what?

A

Often used as part of “progressive combination therapy” for Type 2 DM

35
Q

Glyburide

A

Diabeta, Micronase

Sulfonylureas, Insulin Secretagogues

36
Q

Insulin Secretagogues do what?

A

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

37
Q

Glimepiride

A

Amaryl

Sulfonylureas, Insulin Secretagogues

38
Q

Glipizide

A

Glucotrol

Sulfonylureas, Insulin Secretagogues

39
Q

Nateglinide

A

Starlix

Glinides, Insulin Secretagogues

40
Q

Repaglinide

A

Prandin

Glinides, Insulin Secretagogues

41
Q

Insulin Sensitizers do what?

A

*Increase peripheral cellular sensitivity to
insulin without increasing insulin secretion
Two types: Biguanides and Thiazolidinediones

42
Q

Metformin

A

Glucophage

Biguanides, Insulin Sensitizers

43
Q

Pioglitazone

A

Actos

Thiazolidinediones, Insulin Sensitizers

44
Q

Rosiglitazone

A

Avandia

Thiazolidinediones, Insulin Sensitizers

45
Q

Biguanides prevents what?

A

Prevents hepatic gluconeogenesis (huh?)

***This is very important because hepatic glucose production is the main source of excessive glucose in Type-2 DM!

46
Q

Thiazolidinediones do what?

A

Increase intracellular receptors in skeletal muscle, liver, and adipose tissue to become more sensitive to endogenous insulin.

47
Q

α-Glucosidase Inhibitors (2)

A

Acarbose (Precose)

Miglitol (Glyset)

48
Q

α-Glucosidase Inhibitors work by inhibiting what? which delays what?

A

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.

49
Q

α-Glucosidase Inhibitors cause hypoglycemia??

A

Don’t cause hypoglycemia by themselves, but will contribute significantly in combination RX

50
Q

Saxagliptin

A

Onglyza

Dipeptidyl Peptidase-IV Inhibitors

51
Q

Sitagliptin

A

Januvia

Dipeptidyl Peptidase-IV Inhibitors

52
Q

Miglitol

A

(Glyset)

α-Glucosidase Inhibitors

53
Q

Acarbose

A

(Precose)

α-Glucosidase Inhibitors

54
Q

Sodium Glucose Co-Transporter Inhibitor

SGLT Inhibitor

A

Canagliflozin (Inkovana)

Only one is currently approved for use in the U.S.

55
Q

Inkovana

A

Canagliflozin

Sodium Glucose Co-Transporter Inhibitor
SGLT Inhibitor

56
Q

Dapagliflozin what is it and what is unique about it?

A

(Farxiga)
Sodium Glucose Co-Transporter Inhibitor
(SGLT Inhibitor)
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

Pharm Final (6 decks)

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