Brainscape's Knowledge GenomeTM

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


See full index

Duke Pharmacology- Hannah > Diabetes and Insulin > Flashcards

Diabetes and Insulin Flashcards

1
Q

Endogenously insulin is produced in

A

the beta cells

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

Endogenously glucagon is produced in

A

the alpha cells

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

Insulin promotes

A

storage of glucose, fatty acids, and amino acids

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

daily insulin secreted is equivalent

A

to 40-50 units

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

Activation of Na+/K+ ATPase in cell membranes by insulin

A

moves K+ into cells and decreases concentration of K+ in plasma

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

The primary source of endogenous glucose production following glycogenolysis and gluconeogenesis is

A

the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is insulin secretion regulated?

A

via negative feedback effect of the blood glucose concentration in the pancreas

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

Glycogenesis is

A

glycogen formation

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

Glycogenolysis is

A

glycogen breakdown

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

The body will not secrete insulin when

A

blood glucose levels <50 mg/dL

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

The body secretes maximum insulin at concentrations of

A

> 300 mg/dL

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

Blood glucose concentrations are

A

maintained within a narrow range

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

____ glucose is more effective than ____ glucose in evoking the release of insulin

A

Oral, IV

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

Insulin receptor expression is

A

highest in the tissues

promotes use of carbohydrates for energy

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

Relationship between glucagon and insulin

A

They are reciprocally secreted

glucagon acts to mobilize glucose, fatty acids, and amino acids into systemic circulation

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

Glucagon secretion occurs

A

during hypoglycemia

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

Glucagon acts by

A

activating adenylate cyclase for cAMP formation

exogenous administration can lead to enhanced myocardial contractility

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

Diabetes mellitus can affect vascular system because

A

it impairs vasodilation–> chronic proinflammatory, prothrombic and proatherogenic state–> vascular complications

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

Goals of therapy for diabetes

A

prevent adverse consequences of hypo/hyperglycemia
avoid weight gain
reduce micro/macrovascular complications
HbA1c <6-7% associated with fewer microvascular complications
symptoms often resolve when blood glucose < 200 mg/dL

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

Diagnosis of diabetes is based on

A

elevated fasting plasma glucose greater than 126 mg/dL or hemoglobin of 6.5% or greater

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

Long term complications of diabetes include

A

retinopathy, kidney disease, HTN, CAD, peripheral/cerebral vascular disease, and peripheral/autonomic neuropathies

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

T1DM diagnosis is based on

A

random glucose >200 mg/dL + HbA1C >7%

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

Hypoglycemia treatment

A

each 1 mL of 50% glucose will increase blood glucose of 70 kg patient by 2 mg/dL

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

Hyperosmolar nonketotic coma is due to

A

dehydration/hyperosmolality

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

DKA is

A

decreased insulin activity allows catabolism of free fatty acids into ketone bodies leading to accumulation
infection is a common precipitating factor
Treatment: correct hypovolemia, hyperglycemia and total body potassium deficit

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

The treatment for type 1 DM

A

insulin therapy (necessary for survival)

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

Circulating insulin levels are altered more by

A

renal dysfunction than hepatic disease

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

The duration of action of insulin is

A

30-60 minutes after IV administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Alpha-adrenergic stimulation will

A

decrease basal secretion of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Beta-adrenergic or parasympathetic nervous system will

A

increase basal secretion of insulin

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

Insulin response to glucose is greater after

A

oral ingestion than IV infusion

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

Type 1 DM need

A

at least two daily SQ injections of intermediate or long-acting insulin + rapid acting insulin following meals

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

The basic principle of insulin administration is to

A

provide slow, long-acting, continuous supply of insulin that mimics basal secretion

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

Insulin formulations include:

A

basal insulin-intermediate acting & long acting
short acting- meal time
rapid acting- meal time (preferred for prandial coverage)

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

The most commonly used commercial preparation of insulin is

A

U-100 (100 U/mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Typical daily exogenous dose for T1Dm is around

A

0.5 to 1 U/kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Insulin requirements can be increased dramatically by

A

stress, sepsis, or trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Rapid acting insulins include:

A

lispro, insulin aspart, and glulisine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

The onset, peak and duration for rapid acting insulin is

A

onset: 5-15 minutes, peak 45-75 minutes, duration 2-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Intermediate acting insulins include

A

NPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The onset, peak, and duration for intermediate acting insulin is

A

2 hours, peak 4-12 hours, duration 18-28 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Short acting insulin includes

A

regular insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

The onset, peak, and duration for short acting insulin

A

onset: 30 minutes, peak 2-4 hours, duration 6-8 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Long acting insulins include

A

glargine and detemir (have a similar onset, peak, and duration to intermediate acting insulins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What preparations are used in continuous subcutaneous insulin infusions?

A

short acting (regular) or rapid acting (lispro, aspart, glulisine)

46
Q

CSII or continuous subcutaneous insulin infusion pumps

A

are smart and deliver basal infusion and bolus doses before meals, can accommodate nocturnal basal requirements, pumps are very smart and can alter infusion during exercise, surgery, etc.

47
Q

Type, onset, peak, and duration of action of lispro

A

Lispro or humalog is rapid acting, has an onset of 15 minutes, peak of action of 45-75 minutes, duration of 2-4 hours

48
Q

Benefits of lispro include

A

decrease in postprandial hyperglycemia and less risk of hypoglycemia

49
Q

Lispro has a lysine/proline switch that prevents hexamer formaiton and

A

the monomer is rapidly absorbed
(insulin has 6 molecules that associate with zinc molecules to form hexamers–> must dissociate to monomers before absorption from SQ site)

50
Q

Type, onset, peak, and duration duration of action of insulin aspart and glulisine

A

rapid acting insulin
onset: 10-15 minutes
peak: 45-75 minutes
Duration: 2-4 hours

51
Q

Regular insulin is a

A

short acting insulin (fast-acting preparation) and can only be given IV and subcutaneous

52
Q

Regular insulin also goes by

A

humulin R, Novolin R, ReliOn R

53
Q

What is the preferred treatment for abrupt onset of hyperglycemia or ketoacidosis?

A

regular insulin

54
Q

What is the onset, peak, and duration of action of regular insulin?

A

onset: 30 minutes
peak: 2-4 hours after SQ injection b/c of insulin hexamers
duration: 6-8 hours
periop dosage is 1-5 U or infusion (0.5-2.0 U/hr)

55
Q

What is neutral protamine hagedorn (NPH) and the onset, peak, and duration?

A

intermediate acting
onset: 2 hour
peak: 4-12 hours
duration 18-28 hours

56
Q

What is the onset, peak, and duration of detemir (levemir)?

A

long-acting insulin analogue for basal replacement
onset: 2 hours
peak: 3-9 hours
duration: 6-24 hours
can be administered as single bedtime injection to provide basal insulin for 24 hours with less nocturnal hypoglycemia
cannot be mixed with rapid acting insulin

57
Q

What is the onset, peak, and duration of glargine (lantus)?

A 
long-acting insulin
onset: 90 minutes
peak: none
duration: 20-24+ hours 
less pronounced peaks
58
Q

What is the onset, peak, and duration of degludec (Tresiba)?

A 
long-acting insulin
onset: 2 hours
Peak: none
duration: > 40 hours 
can be used in hepatic/renal impairment
59
Q

For mixed insulins, the first number is

A

long acting and the second is the short/rapid acting insulin
always dosed before breakfast and evening meal

60
Q

What are the five main side effects of insulin?

A

hypoglycemia, allergic reactions, lipodystrophy, insulin resistance, and drug interactions

61
Q

The most serious side effect of insulin is

A

hypoglycemia
first symptoms are compensatory effects of increased epinephrine secretion: diaphoresis, tachycardia, HTN, rebound hyperglycemia caused by SNS activation may mask diagnosis (Somogyi effect)

62
Q

What is the Somogyi effect?

A

when there is rebound hyperglycemia caused by SNS activation during a period of hypoglycemia

63
Q

Why do we have severe CNS effects with hypoglycemia & what are they?

A

mental confusion, seizures, and coma because brain depends on glucose for metabolism

64
Q

Prolonged hypoglycemia can cause

A

irreversible brain damage

65
Q

What is lipodystrophy?

A

fat atrophies at site of SQ injection

66
Q

Insulin resistance is

A

when a patient requires more than 100 units of insulin daily
acute insulin resistance is associated with trauma from infection/surgery

67
Q

It is necessary to be mindful of allergic reactions with

A

NPH & heparin b/c protamine could be administered IV to antagonize anticoagulant effects of heparin and cause large allergic reaction to protamine

68
Q

What are the four major classes of oral antidiabetic drugs?

A

secretagogues, biguanides, thiazolidinediones or glitazones, and alpha-glucosidase inhibitors

69
Q

Secretagogues include

A

sulfonylureas and meglitinides and increase insulin availability

70
Q

Biguanides include

A

metformin and suppress excessive hepatic glucose release

71
Q

Thiazolidinediones or glitazones include

A

rosiglitazone, pioglitazone and improve insulin sensitivity

72
Q

Alpha-glucosidase inhibitors include

A

acarbose, miglitol and delay GI glucose absorption

73
Q

Metformin is

A

an oral biguanide

rarely causes hypoglycemia & can be used in combination with insulin and sulfonylureas

74
Q

Contraindications of metformin include

A

lactic acidosis, AKI, GI intolerance, acute hepatic disease

caution in patients with renal dysfunction d/t dependence on renal clearance

75
Q

Where is metformin metabolized?

A

it is not; it is excreted by the kidneys

76
Q

Metformin can also be used

A

in PCOS, nonalcoholic fatty liver, premature puberty

77
Q

The elimination half-time of metformin is

A

2 to 4 hours

78
Q

The dosage of metformin is

A

TID 500-1000 mg w/ meals

79
Q

The mechanism of action of metformin is

A

activates adenosine monophosphate activated protein kinase to suppress hepatic glucose production

80
Q

Metformin should not be administered in patients with

A

hepatic dysfunction, renal insufficiency (creatinine >1.5 mg/dL), IV contrast dye, acute MI, CHF, arterial hypoxemia, and sepsis b/c it can cause lactic acidosis

81
Q

Metformin should be discontinued

A

48 hours before elective surgery because of its ability to cause lactic acidosis

82
Q

Sulfonylureas should not be administered to

A

patients with sulfa allergies

83
Q

The mechanism of action of sulfonylureas are

A

to act on sulfonylurea receptors on pancreatic and cardiac cells; inhibit adenosine triphosphate sensitive K+ channels on pancreatic beta cells resulting in Ca2+ influx and simulation of insulin resistance

84
Q

Sulfonylureas produce

A

hypoglycemia that is infrequent but is more often prolonged and more dangerous than hypoglycemia from insulin

85
Q

Sulfonylureas have a cardioprotective mechanism through

A

close K-ATPase channels and inhibit ischemic preconditioning

86
Q

Glyburide is considered a ____ and it’s mechanism of action is

A

sulfonylurea and it increases insulin sensitivity and inhibits liver production of glucose

87
Q

What is the dose, peak plasma level, DOA, elimination half-time of glyburide?

A

dose: 2.5-20 mg daily (Qd/BID)
Peak plasma: 3 hours
DOA: 18-24 hours
Elimination half-time: 4.6-12 hours

88
Q

Where is glyburide metabolized?

A

liver

89
Q

What is the dosage, duration of action, and elimination half-time of glipizide?

A

sulfonylurea
dose: 5-40 mg daily
duration of action: 12-24 hours
elimination half-time: 4-7 hours

90
Q

What is the dosage, duration of action, and elimination half-time for glimepiride?

A

sulfonylurea
dose: 2-4 mg daily
duration of action: 24+ hours
elimination half-time: 5-8 hours

91
Q

Meglitinides include

A

repaglinide and nateglinide and are secretagogues

92
Q

A concern with nateglinide (Starlix) includes

A

accumulation of active metabolites may cause hypoglycemia

93
Q

The mechanism of action of meglitinides include

A

stimulation of release of insulin from the pancreas

94
Q

Alpha-glucosidase inhibitors include

A

acarbose and miglitol and work by decreasing carbohydrate digestion and absorption of disaccharides by interfering with intestinal glucosidase activity

95
Q

Thiazolidinediones include

A

rosiglitazone and pioglitazone and they act at skeletal muscle, liver, and adipose tissue via peroxisome proliferator activator receptor-gamma to decrease insulin resistance and hepatic glucose production and to increase use of glucose by the liver

96
Q

glucagon like peptide-1 receptors agonists include

A

exenatide and liraglutide and they bind to receptors in the pancreas, GI tract, and brain to increase insulin secretion from beta cells (glucose dependent), decrease glucagon production from alpha cells and reduce gastric emptying

97
Q

Dipeptidyl-peptidase- 4 inhibitors include

A

Saxagliptin, sitagliptin, linagliptin, alogliptin, and vildagliptin and increase insulin secretion from alpha cells (glucose dependent) and reduce pancreatic alpha cell secretion of glucagon

98
Q

Amylin agonists include

A

pramlintide and it does not alter insulin levels

it suppresses gastric emptying, inhibits glucagon release and reduces HbA1c levels

99
Q

Colesevalam acts as

A

a bile acid sequestrant and lowers glucose levels and decreases HbA1C (MOA unclear)

100
Q

Bromocriptine mesylate is

A

a dopamine receptor agonist and it lowers glucose levels and decreases HbA1c (MOA unclear)

101
Q

What are the aims of combination therapy?

A

target two or more causes of hyperglycemia simultaneously
Primary aim: decrease HbA1c
Secondary aim: decrease in daily insulin dose

102
Q

Diabetic autonomic neuropathy is

A

a decreased ability to compensate/risk of CV instability/sudden cardiac death
patients with DM and HTN have 50% likelihood

103
Q

Patients with diabetes are at risk for aspiration due to

A

autonomic dysfunction–> delayed gastric emptying–> premedicate with antacid and metoclopramide

104
Q

Perioperative morbidity in diabetic patients is

A

related to their preexisting end-organ damage

105
Q

Glucose should be kept at

A

<180 intraop

106
Q

Patients with T1DM may have difficult intubations because

A

of temporomandibular joint and spine mobility should be assessed preoperatively to assess for glycosylation of tissue proteins and limited mobility of joints

107
Q

Hyperglycemia is associated with:

A

hyperosmolarity, infection, poor wound healing, increased mortality
severe hyperglycemia–> worse neurological outcomes following ischemia

108
Q

Plasma glucose levels should be

A

monitored q30-1 hour intraop with insulin infusions and diabetic patients in general

109
Q

____ & ____ should be held prior to surgery

A

sulfonylureas and metformin have long half-lives and should be discontinued 24-48 hours before surgery

110
Q

One unit of regular insulin lowers plasma glucose by

A

25-30 mg/dL

111
Q

Regular insulin-units per hour=

A

plasma glucose/150 (this is so dumb to memorize)

112
Q

AM dose of regular insulin

A

should be held the day of surgery

Duke Pharmacology- Hannah (14 decks)

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