Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 4: Diabetes Pharmacology > Flashcards

Exam 4: Diabetes Pharmacology Flashcards

You may prefer our related Brainscape-certified flashcards:
NCLEX-PN® flashcards NCLEX-RN® flashcards
1
Q

Two reasons for hyperglycemia in DMII:

A

Lack of insulin production once β cells fail

Cells resistant to insulin action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Insulin produced by:

A

β cells in islets of Langerhans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

β cells secrete insulin in response to:

A

↑ circulating glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Insulin released as:

A

Proinsulin (precursor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Structure of insulin:

A

Small protein chain of 21 amino acids linked by two disulfide bridges to a β chain of 30 amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effects of insulin:

A 
Glucose into cells
Glycogen creation
Uptake of amino acids, Phos, K, Mg
Protein synthesis/inhibited proteolysis
Fatty acid/TG synthesis
↓ lipolysis
DNA/gene regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Portal circulation receives basal insulin rate of:

A

1U/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

With meals, insulin secretion increases:

A

5-10x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Average daily requirement of insulin:

A

40U

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ANS influence on insulin secretion:

A

α stimulation ↓ insulin

β and PSNS stimulation ↑ insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

History of making insulin:

A

Stage 1: insulin extracted from pigs/cows
Stage 2: replaced one ‘wrong’ amino acid to make it identical to human
Stage 3: Make yeast or e.coli produce it instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rapid-acting forms of insulin:

A

Lispro (Humalog)
Aspart (Novalog)
Glulisine (Apidra)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Short-acting form of insulin:

A

Regular (Humulin R/Novolin R)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Intermediate-acting form of insulin:

A

NPH (Humulin N/Novolin N)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Long-acting forms of insulin:

A

Glargine (Lantus)
Detemir (Levemir)
Ultralente

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Delivery forms for insulin:

A

SQ
IV
Inhaled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Insulin mixtures available:

A

R/NPH

Rapid/NPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Long-acting insulin used to mimic:

A

Basal insulin rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Insulin mixture incompatibilities:

A

Do not mix glargine with others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

PK of IV regular insulin:

A

E1/2t of IV bolus: 5-10 min
Duration: 30-60 minutes
Metabolized in liver/kidneys by proteolytic enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Insulin’s relatively long duration is due to:

A

Tightly binding to receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Formulation to use IV:

A

U-100 (100 units/ml)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Onset/peak/duration of rapid-acting insulin (lispro):

A

Onset: 10-15 min
Peak: 30-60 min
Duration: 3-5 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Onset/peak/duration of short-acting insulin (regular):

A

Onset: 30-60 min
Peak: 1-5 hrs
Duration: 5-8 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Onset/peak/duration of intermediate-acting insulin (NPH):

A

Onset: 1-2 hrs
Peak: 6-10 hrs
Duration: 16-20 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Onset/peak/duration of long-acting insulin (glargine):

A

Onset: 2-6 hrs
Peak: none
Duration: 24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Delivery methods for insulin:

A

Syringe
Pens
Jet injectors
Insulin pumps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

A/E of insulin injection:

A 
Site rxns
Lipodystrophy at site
Protamine allergy
Weight gain
Hypoglycemia!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

S/s of hypoglycemia:

A 
Diaphoresis
Tachycardia
HTN
CNS agitation
Seizures
Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Drugs that oppose the hypoglycemic effects of insulin:

A

ACTH
Glugacon
Estrogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Drug that decreases insulin release/mobilizes glucose:

A

Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Drugs that prolong insulin duration:

A

Tetracycline
Chloramphenicol
Salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Drugs that increase hypoglycemic effects of insulin:

A

MAOIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In a type I diabetic 1 U will ↓ BG by:

A

40-50 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

In a type II diabetic 1 U will ↓ BG by:

A

30-40 mg/dL

36
Q

Advantages of tight periop BG control:

A

↑ healing

↓ infection, diuresis, DKA

37
Q

Disadvantages of tight periop BG control:

A

Hypoglycemia risk without labor intensive monitoring/adjustments

38
Q

Nontight periop managment of diabetes:

A

D5W @ 100-125cc/hr in 2nd IV
30-50% of normal AM intermediate insulin
Check BG q1-2hr, adjust D5W
SS insulin for BG > 200-250

39
Q

Tight periop management of diabetes:

A

D5W @ 100-150cc/hr in 2nd IV
50U regular insulin in 250cc NS piggybacked
Insulin rate: (last BG/150)/hr
** BG/100 for steroids, obese, infection
Add 20mEq K+ for each liter of glucose infused

40
Q

Tx of hyperkalemia:

A

10U regular insulin IV
25g glucose
1 amp D50
Over 5 minutes

41
Q

Tx of hypoglycemia:

A

Conscious: Fast acting oral sugar
Anesthetized: 25-50ml D50

42
Q

MoA of sulfonylureas:

A

Stimulates release of insulin from β cells (binds to ATP sensitive K+ channels that allow depolarization)

Enhances β cell sensitivity to glucose
Enhances tissue sensitivity to insulin
Normalizes hepatic glucose production

43
Q

FBG, A1c reduction with sulfonylureas:

A

60-70 mg/dL

Up to 2%

44
Q

1st generation sulfonylureas:

A

Tolbutamide

Chlorpropamide

45
Q

2nd generation sulfonylureas:

A

Glipizide
Glyburide
Glimepiride

46
Q

1st vs 2nd generation sulfonylureas:

A

1st has more drug interactions/SE than 2nd

2nd 100x more potent but no more effective

47
Q

PK of sulfonylureas:

A

90-98% protein bound

Hepatic metabolism

48
Q

Renal impairment best served by these sulfonylureas:

A

Glipizide or tolbutamide

49
Q

A/E of sulfonylureas:

A

GI: nausea, fullness, cholestasis, LFTs, appetite stim
GU: ADH-like effect
Derm: pruritis, rash
Hypoglycemia

50
Q

Pre-op mgmt of sulfonylureas:

A

Hold 24-48 hrs preop

51
Q

MoA of sulfonylureas:

A

Stimulates release of insulin from β cells (binds to ATP sensitive K+ channels that allow depolarization)

Enhances β cell sensitivity to glucose
Enhances tissue sensitivity to insulin
Normalizes hepatic glucose production

52
Q

Class and MoA of metformin:

A

Biguanide

Decreases hepatic and renal glucose production

Enhances insulin receptor binding
Increases glucose utilization, decreases insulin resistance
Requires insulin to work!

53
Q

Clearance of metformin:

A

Excreted unchanged by kidneys

54
Q

FPG change from metformin:

A

60 mg/dL

More with sulfonylureas

55
Q

Benefits of metformin:

A

No weight gain
May ↑ HDL, ↓ LDL/TG
Hypoglycemia rare

56
Q

A/E of metformin:

A

GI: diarrhea, metallic taste, nausea
Lactic acidosis
Rash

57
Q

Contraindications for metformin:

A

ESRD: ♀ Cr > 1.4, ♂ Cr > 1.5
Hepatic dysfunction
CHF, shock, hypoxic pulm disease

58
Q

Examples of thiazolidinediones:

A

Pioglitazone (Actos)

Rosglitazone (Avandia)

59
Q

MoA of thiazolidinediones:

A

Improves insulin sensitivity/decreases insulin resistance

Reduces hepatic glucose production

60
Q

FBG/A1c changes with thiazolidinediones:

A

FBG ↓ 50 mg/dL

A1c ↓ 1-2%

61
Q

Clearance of thiazolidinediones:

A

Hepatic metabolism

62
Q

Unique advantage of thiazolidinediones:

A

Will restore ovulation in women who had stopped due to insulin resistance

63
Q

A/E of thiazolidinediones:

A

Edema
Weight gain
Hepatotoxicity

64
Q

Black box warnings for thiazolidinediones:

A

CHF - cause or exacerbate

Possible MI with rosiglitazone

65
Q

Examples of alpha-glucosidase inhibitors:

A

Acarbose (Precose)

Miglitol (Glyset)

66
Q

MoA of alpha-glucosidase inhibitors:

A

Antagonizes enzymes in brush border that digest complex carbs to delay glucose absorption and lower post-prandial hyperglycemia

67
Q

FBG/PPG/A1c changes with alpha-glucosidase inhibitors:

A

FBG ↓ 25-30
PPG ↓ 60-70
A1c ↓ 0.7 - 0.9%

68
Q

Clearance of alpha-glucosidase inhibitors:

A

Excreted in stool

69
Q

A/E of alpha-glucosidase inhibitors:

A

Abdominal pain/distention
Diarrhea
Flatulence

70
Q

Considerations with alpha-glucosidase inhibitors:

A

Take with first bite of meal

Caution with IBD, colon ulceration, obstruction

71
Q

Examples of meglitinides:

A

Repaglinide (Prandin)

Nateglinide (Starlix)

72
Q

MoA of meglitinides:

A

Stimulates insulin secretion from β cells

73
Q

PK of meglitinides:

A

Onset and peak: 1 hr

Duration: 4 hrs

74
Q

Administration of meglitinides:

A

Take 15-30 min before meals
Skip meal - skip dose
Add meal - add dose

75
Q

A/E of meglitinides:

A

Hypoglycemia
N/V/C/D, heartburn
Headache

76
Q

MoA of gliptins:

A

Inhibit DPP-4, which stimulates GLP-1, which enhances glucose-dependent insulin secretion

77
Q

Example of gliptins:

A

Sitagliptan (Januvia)

78
Q

PK of sitagliptan:

A

E1/2t: 12 hours

79
Q

Efficacy of gliptins:

A

Modest; third-line drug

80
Q

A/E of gliptins:

A

Rare fatal pancreatitis, anaphylaxis

81
Q

MoA of exenatide:

A

GLP-1 analog; identical MoA to gliptins

82
Q

A/E of exenatide:

A 
N/V
Antibody development
Pancreatitis (can be fatal)
Transplant-requiring renal failure 
Hypersensitivity
Delayed gastric emptying
83
Q

MoA of pramlintide:

A

Analog of amylin that ↓ gastric emptying, glucagon secretion, and ↑ feeling of satiety

84
Q

PK of pramlintide:

A

Peak: 20 min post-SC injection
E1/2t: 49 minutes
Metabolized in kidneys

85
Q

Indications for pramlintide:

A

Enhance insulin effects in DM I/II patients who cannot control well with insulin

86
Q

A/E of pramlintide:

A

Hypoglycemia
Nausea
Site rxns
Decreased absorption of drugs

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions