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Pharmacology > Pharm 18- Diabetic Drugs > Flashcards

Pharm 18- Diabetic Drugs Flashcards

1
Q

Where is the pancreas found?

A

“Tucked in” the angle formed by the gastric pylorus and the proximal duodenum

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2
Q

Two functions of the pancreas

A

Exocine (various digestive enzymes)

Endocrine

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3
Q

What does the endocrine pancreas produce?

A 
Insulin ("fed" state)
Glucagon ("hungry" state)
Gastrin
Somatostatin
Many others
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4
Q

What secretes insulin?

A

Beta cells

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5
Q

What does insulin do?

A

causes blood glucose to go down (fed state, you want to stash that energy)

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6
Q

What do alpha cells do? Where are they?

A

Endocrine pancreas; secrete glucagon which causes blood glucose to go up

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7
Q

What do delta cells do? Where are they?

A

Endocrine pancreas; secrete somatostatin which regulates a lot of things

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8
Q

What does the exocrine pancreas release?

A

Bicarb and digestive zymogens to break down fats and proteins

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9
Q

Two types of Diabetes

A

Diabetes insipidus

Diabetes mellitus

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10
Q

What is diabetes insipidus?

A

Doesn’t produce or kidneys don’t respond to vasopressin (ADH); produces a lot of dilute urine no matter how hydrated you are

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11
Q

What are the types of diabetes mellitus?

A

Type 1
Type 2
Type 3 “Other” DM
Gestational DM

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12
Q

All DM is characterized as an ___________ or _________ deficiency of what?

A

Absolute; relative; insulin

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13
Q

Type 1 DM

A

Insulin-Dependent DM (IDDM)

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14
Q

Type 2 DM

A

Non-Insulin Dependent DM (NIDDM)

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15
Q

What is an absolute insulin deficiency?

A

Type 1 DM

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16
Q

What is a relative insulin deficiency?

A

Type 2 DM

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17
Q

What type of diabetes is classically childhood diabetes?

A

Type 1

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18
Q

Age of Onset: Type 1 vs Type 2

A

Type 1: Usually during childhood or puberty

Type 2: Commonly over age 35

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19
Q

Nutritional status at time of onset: Type 1 vs Type 2

A

Type 1: Commonly undernourished

Type 2: Obesity usually present

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20
Q

Prevalence: Type 1 vs Type 2

A

Type 1: 5-10% of diagnosed diabetics

Type 2: 90-95% of diagnosed diabetics

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21
Q

Genetic predisposition: Type 1 vs. Type 2

A

Type 1: Moderate

Type 2: Very strong

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22
Q

Defect of deficiency: Type 1 vs Type 2

A

Type 1: B cells destroyed, eliminate production of insulin

Type 2: Inability of B cells to produce appropriate quantities of insulin; insulin resistance; other defects

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23
Q

Which type of diabetes must receive insulin?

A

Type 1

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24
Q

What are the 4 “Classic” symptoms of Type 1 DM

A
  1. Polyphagia (eat a lot)
  2. Polyuria (urinate a lot)
  3. Polydipsia (drinking)
  4. Weight loss
    Others (wounds wont heal, sexual dysfunction, blurred vision bc glucose builds up, etc)
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25
Q

Which type of diabetes produce variable amounts of insulin and exhibit insulin resistance?

A

Type II DM

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26
Q

What type of therapy does Type II DM typically require?

A

Increasing doses of insulin and combination therapy with other antihyperglycemics

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27
Q

What causes Type 3 DM: “Other”? What is the course/tx?

A

Due to side effects of drugs, toxins, viral infections, genetic predisposition, etc.; variable in course/treatment

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28
Q

When could Type 4 DM: Gestational occur?

A

Women may develop extreme insulin resistance during their third trimesters of pregnancy as a result of hormone changes

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29
Q

How is Type 4 Diabetes controlled?

A

Controlled with insulin

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30
Q

What happens is Type 4 diabetes is not controlled?

A

Can lead to extremely large babies, dystocia, and neonatal hypoglycemia

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31
Q

Dystocia

A

difficult birth, typically caused by a large or awkwardly positioned fetus, by smallness of maternal pelvis or by failure of uterus and cervix to contract and expand normally

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32
Q

What is insulin?

A

A small polypeptide consisting of two chains (A and B) connected by a disulfide bond.

33
Q

What is the half-life of insulin?

A

3-5 minutes

34
Q

Why are plasma insulin levels not an accurate measure of insulin production?

A

REmoved from the circulation so rapidly (3-5 minutes)

35
Q

What is a better guide for insulin production?

A

C-protein measurement

36
Q

C-Protein

A

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

37
Q

What is the half-life of C-protein?

A

30 minutes

38
Q

How many x as much insulin in the blood stream?

A

5x as much in the blood stream

39
Q

What produces insulin?

A

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

40
Q

What does insulin’s main effect target tissues?

A

Liver, fat, muscle

41
Q

Insulin exhibits ________ effects on target tissues.

42
Q

Anabolic

A

construct molecules from smaller units

43
Q

What is insulin increasingly being used for by perfusionists? In conjunction with what?

A

Hyperkalemia therapy

Often in conjunction with glucose to drive potassium intracellularly

44
Q

What else can you do to lower potassium levels?

A

Dialysis (not really on bypass)
Z buf; hemoconcentrator
Bicarb will drive potassium intracellularly

45
Q

What types of protocols have become more common since perfusionists have started to seek much “Finer” control of glucose levels on bypass?

A

Insulin drip and anti-hyperglycemic protocols

46
Q

Types of insulin (Rapid onset/ short acting)

A 
Regular insulin (Humulin R, Novolin R)
Insulin aspart (Novolog)
Insulin glulisin (Apidra)
Insulin Lispro (Humalog)

Given IV or SQ

47
Q

What insulin can be given IV on bypass?

A

Regular insulin (Humulin R, Novolin R)

48
Q

Types of insulin (Intermediate onset)

A

Neutral Protamine Hagedorn (NPH) insulin
(Humulin N, Novolin N)
Only given SQ

49
Q

Types of insulin (long acting)

A 
Insulin glargine (Lantus)
INsulin detemir (Levemir)

Do not mix with other types of insulin

50
Q

Fatty-acid side-chain attachments allow long acting insulins to do what?

A

Cause them to bind albumin for longer action

51
Q

What is the goal of various mixtures compatible insulin?

A

MInimize hyper- and hypoglycemia

52
Q

ADA recommends diabetics’ blood glucose (BG) maintain a mean of what?

53
Q

Long-term BG measurement is via what?

A

Glycated (Glycosylated) Hb (HbA1c)

54
Q

Normal HbA1c

55
Q

DM target

56
Q

Injectable Antihyperglycemics

A

Pramlintide (Symlin); B-cells in the islets of langerhans made this

57
Q

What is Amylin?

A

A polypeptide released by the pancreas in conjuction with insulin

58
Q

How does Amylin work?

A

With insulin to moderate physiologic glucose levels by slowing gastric emptying and digestion

59
Q

Why is it important for digestion to be slowed in regards to Pramlintide (Symlin)?

A

Slow digestion allow Pramlintide (Symlin) to spread out glucose absoprtion over a longer period

60
Q

How is Pramlintide (Symlin) given?

A

SQ at meals

61
Q

What does Pramlintide (Symlin) cause?

A

Post-prandial satiety which has potential for future uses

62
Q

What are examples of Incretin Mimetics?

A

Exenatide (Byetta) - Short acting
Liraglutide (Victoza) - Long acting

Both given SQ prior to eating; side effects:GI

63
Q

What are incretins?

A

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

64
Q

What are oral Insulin “Adjuncts”?

A

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

65
Q

What are some oral insulin “Adjunct” examples?

A 
Insulin Secretagogues
Insulin Sensitizers
Alpha-Glucosidase Inhibitors
Dipeptidyl Peptidase IV inhibitors
Sodium Glucose Co-Transporter Inhibitors (SGLT Inhibitors)
66
Q

How do insulin secretagogues work?

A

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

67
Q

How do insulin sensitizers work?

A

Increase peripheral cellular sensitivity to insulin without increasing insulin secretion

68
Q

What do Biguanides work?

A

Prevents hepatic gluconeogenesis; this is very important because hepatic glucose production is the main source of excessive glucose in Type 2 DM

69
Q

What are biguanides often used in combination with?

A

Insulin or other oral antiglycemics

70
Q

What is a very common side effect with biguanides?

71
Q

Thiazolidinediones

A

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

72
Q

What are side effects of thiazolidinediones?

A

Weight gain, liver damage, and increased CV risks

73
Q

How do alpha-glycosidase inhibitors work?

A

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 the combination RX

74
Q

How do dipeptidyl peptidase-IV inhibitors work?

A

Work at the cellular level to increase post-prandial insulin release while inhibiting glucagon (insulin’s physiologic antagonist )release

75
Q

SGLT

A

Sodium Glucose Co-Transporter Inhibitors (SGLT Inhibitors)

76
Q

SGLT2

A

Low affinity, high capacity transport mechanism in the proximal tubule; designed to capture glucose lost in the renal filtration

77
Q

SGLT2 Inhibitors

A

Glucose freely lost in the urine with fairly predictable side effects

78
Q

Why was dapaglifozin (Farxiga) not approved in the US?

A

6-fold increase in bladder cancer; but still extensively used in Europe; Astra Zenica got it approved

Pharmacology (23 decks)

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