Antidiabetic Medications Flashcards

1
Q

Which type of diabetes are oral antihyperglycemics commonly used?

A

for type 2 diabetes

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2
Q

7 types of antihyperglycemic?

A

biguanides

sulfonylureas

glinides

thiazolidinediones (glitazones)

a- glucose inhibitors

dipeptidyl- peptidase 4 inhibitors (DPP 4 inhibitors)

sodium-glucose cotransporter 2 inhibitor

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3
Q

Type 2 diabetes pathophysiology (2)

2 common treatment

A

insulin resistance

reduction in B cells

Treatment: lifestyle modification and oral hypoglycemics

lifestyle changes first before drug therapy (smoking cessation, diet, exercise)

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4
Q

Combination therapy is recommended if A1C exceeds?

What is Combination Therapy?

A

9 %

Two drugs from different classes

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5
Q

What is the A1C target?

A

less than 7 %

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6
Q

Effective treatment of TYPE 2 involves several elements: (4)

A

Lifestyle changes

Careful monitoring of blood glucose levels even if in oral medications

Therapy with one or more drugs

Treatment of associated comorbid conditions such as high cholesterol and high blood pressure

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7
Q

New-onset TYPE 2 diabetes treatment

A

Lifestyle interventions 1st

Oral biguanide lifestyle changes not effective

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8
Q

If lifestyle modifications and the maximum tolerated metformin dose do not achieve the recommended A1c goals after 3 to 6 months, additional treatment should be given with ______________ and ___________ or ______________.

A

dipeptidyl peptidase4 (DPP-4) inhibitors

glucagonlike peptide 1 (GLP-1) receptor agonists

Insulin

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9
Q

Insulin and oral hyper glycemic results in (2)

what 2 types of insulin?

A

better glycemic control

weight loss

intermediate or long acting

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10
Q

Diabetes Canada 2018 recommends

A1C of new-onset type 2 diabetes

treatments 2

A

new-onset type 2 diabetes with an A1C of less than 7 % be treated with lifestyle modifications for 2 to 3 months

ADD biguanides (metformin) if lifestyle changes not effective

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11
Q

Biguanides
-drug name
-what kind of therapy
-BMI use

A

metformin

first line drug therapy, BMI over 25

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12
Q

Biguanides mechanism of actions 5

A

Decrease GLUCOSE PRODUCTION in the liver

Decrease INTESTINAL ABSORPTION of GLUCOSE

Decrease liver production of triglycerides & cholesterol

IMPROVE INSULIN RECEPTOR SENSITIVITY- so more insulin can go into the cell

Improves glucose uptake by skeletal muscle, adipose and liver

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13
Q

Biguanides Does not increase insulin secretion from the pancreas and therefore does not cause ________

Biguanides do not cause _____ and _______ because it does not stimulate _______________

A

Does not increase insulin secretion from the pancreas and therefore does not cause hypoglycemia

Biguanides do not cause weight gain and hypoglycemia because it does NOT stimulate insulin production

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14
Q

Biguanides may be used in combination with ______, _______, and ________ when lifestyle measures are not successful

A

May be used in combination with

sulfonylureas
thiazolidinediones
incretin mimetics

when monotherapy & lifestyle measures are not successful

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15
Q

Biguanides adverse effects

A

Abdominal bloating, nausea, cramping, a feeling of fullness, and diarrhea (GI)

Metallic taste, hypoglycemia,

reduction in vitamin B12 levels after long-term use

Lactic acidosis is an extremely rare complication.

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16
Q

Biguanides indications

A

Initial oral drug, cause weight loss

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17
Q

Biguanides contraindications

include medications

A

kidney disease (creatinine <30 ml/min)

  • metformin is excreted by kidneys and can accumulate if not eliminated, which can cause LACTIC ACIDOSIS

FUROSEMIDE
NIFEDIPINE (antihypertensives)
CIMETIDINE
DIGOXIN
(they can increase concentration)

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18
Q

Biguanides Interaction

A

IODINE BASED DYE

IODINATED RADIOLOGICAL CONTRAST which can cause KIDNEY INJURY and lactic acidosis

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19
Q

Discontinue _______ the day of the test and _____ after undergoing radiological study that requires radioactive iodine-based dye

This may lead to _____ and ______

A

Discontinue BIGUANIDES the day of the test and 48 HOURS after undergoing RADIOLOGICAL study that requires radioactive IODINE based DYE

This may leads to acute KIDNEY injury and LACTIC acidosis

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20
Q

What are 6 symptoms of lactic acidosis?

A

hyperventilation, cold and clammy skin, muscle pain, abd pain, irregular HR, dizziness

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21
Q

1 drug of Sulfonylureas

A

GLIclazide (important)

GLYburide
GLImepiride

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22
Q

What does Sulfonylureas need to work?

A

functioning B cells in the pancreas for sulfonylureas to be effective

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23
Q

Sulfonylureas is not used for?

why?

A

Type 1 because they do not have functioning B cells

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24
Q

Sulfonylureas mechanism of actions

A

bind to RECEPTORS on B cells in the pancreas to stimulate insulin

enhance the action of insulin in the liver, adipose and muscle

decrease glucagon secretion

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25
Q

Sulfonylureas is used as

A

a second-generation drug- used after the first line (second line for those A1C remains high after metformin)

oldest antihypergylcemic

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26
Q

Sulfonylureas adverse effects

A

hypoglycemia, weight gain, skin rash, nausea, epigastric fullness, and heartburn

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27
Q

WHAT to do if CBG is less than 4 mmol/L?

A

Hold insulin and oral antihyperglycemic drugs

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28
Q

Once insulin is started, _____ is stopped

A

Sulfonyureas

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29
Q

Sulfonyureas contraindications

A

ALCOHOL (induced vomiting and hypertension)
NPO
allergy to sulfonamide abx
Not used in pregnancy- only give insulin
severe liver and kidney disease

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30
Q

Sulfonyureas - Gliclazide
-onset
-duration
- interactions

A

rapid onset, short duration

Increased effect of hypoglycemia:

ALCOHOL*, anabolic steroids, β blockers, chloramphenicol (abx- meningitis), MAOI’s, oral anticoagulants, sulfonamides, garlic, ginseng

Decreased effect:

Adrenergics, corticosteroids, thiazides, thyroid drugs

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31
Q

Sulfonyureas - Gliclazide mechanism of action

A

stimulate pancreas to secrete insulin

transport excess glucose from blood to cells of muscle, liver, and adipose

has antiplatelet and antioxidant properties

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32
Q

Give Gliclazide- sulfonylureas immediate release

A

30 minutes before meals

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33
Q

1 medication of Glinides

A

Repaglinide

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34
Q

Glinides mechanism of actions

A

increase insulin secretion in the pancreas

Similar with sulfonylureas

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35
Q

Glinides duration of action?

when to give?

A

much shorter duration of action

give with meals

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36
Q

Glinides are useful for diabetics who have?

A

postprandial glucose levels and low insulin levels

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37
Q

Glinides cannot be combined with?

WHY?

A

sulfonylureas because of their similar mechanism of action

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38
Q

Glinides indications:

do not give (2)

A

diabetics with postprandial glucose levels

DO NOT give without meals
DO NOT GIVE with sulfonylureas

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39
Q

Thiazolidinediones: Glitazones

mechanism of actions

1 drug

A

Insulin sensitizing; enhance receptor sensitivity
* enhancing insulin receptor sensitivity > decrease insulin resistance

stimulate glucose uptake and storage

inhibit glucose and triglyceride production in liver

affects gene regulation

preservation of B cell function- slow disease progression

pioglitazone

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40
Q

Thiazolidinediones: Glitazones onset

A

slow onset up to months

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41
Q

1 drug of Thiazolidinediones

Reserved for pt who cannot tolerate or achieve gLucose control with metformin or sulfonylureas. WHY?

A

pioglitazone

due to cost, adverse effect, slow onset

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42
Q

Thiazolidinediones: Glitazones

Contraindications?

A

Heart disease- can worsen heart failure
Kidney/ liver disease

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43
Q

Thiazolidinediones adverse effects

A

peripheral edema

weight gain- water retention and increased adipose tissue

decrease bone density; increase risk for fracture

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44
Q

Thiazolidinediones: Glitazones interactions

A

erythromycin

ketoconazole

increases concentration

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45
Q

1 drug of Dipeptidyl peptidase 4 (DPP-4) Inhibitors

A

sitagliptin - Januvia

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46
Q

incretin hormones

A

increase insulin synthesis and decrease glucagon secretion

released throughout the day, after a meal

stimulate insulin secretion

reduce postprandial glucose production
slow gastric emptying

increase satiety

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47
Q

DPP-4 enzymes

A

metabolize incretin hormones which results in increased glucose

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48
Q

Dipeptidyl peptidase 4 (DPP-4) Inhibitors mechanism of action

A

Delay breakdown of incretin hormone by inhibiting enzyme DPP-4

increase insulin secretion
lower glucagon secretion

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49
Q

Dipeptidyl peptidase 4 (DPP-4) Inhibitors can be combined with?

A

metformin

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50
Q

Dipeptidyl peptidase 4 (DPP-4) Inhibitors indicators

A

adjunct to changes in diet and exercise habits to increase glycemic control

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51
Q

Dipeptidyl peptidase 4 (DPP-4) Inhibitors adverse effects

A

upper respiratory tract infection
headache
dizziness
hypopglycemia

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52
Q

Dipeptidyl peptidase 4 (DPP-4) Inhibitors contraindication

A

digoxin- increase levels

sulfonylureas

insulin

CYP3A4 inducers- carbamazepine, dexamethasone, phenobarbital, phenytoin, rifampin)

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53
Q

Sodium Glucose Cotransporter 2 Inhibitors: mechanism of actions

A

A decrease in blood glucose caused by an increase in RENAL GLUCOSE EXCRETION

Action: work independently of insulin to prevent glucose reabsorption from the glomerular filtrate, resulting in a reduced renal threshold for glucose and glycosuria

Other effects: may increase insulin sensitivity and glucose uptake in the muscle cells and decrease gluconeogenesis (use of glucose)

Results: improved glycemic control, weight loss, and a low risk of hypoglycemia

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54
Q

1 medication of Sodium Glucose Cotransporter 2 Inhibitors

A

canaglifozin (Invokana®), dapaglifozin (Forxiga®) > osmotic diuresis > intravascular volume depletion

a new class (2014) of oral drugs for the treatment of type 2 diabetes.

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55
Q

Sodium Glucose Cotransporter 2 Inhibitors: ADVERSE effects

A

vaginal yeast infections and UTIs due to increase glucose in those areas

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56
Q

Sodium Glucose Cotransporter 2 Inhibitors

What is the sodium-glucose cotransporter?

Inhibiting it results in?

A

inhibits sodium-glucose cotransporter (which is a protein that facilitates 90% of glucose reabsorption in kidneys)

reduce glucose

kidney glucose excretion is increased

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57
Q

Sodium Glucose Cotransporter 2 Inhibitors contraindication

interactions

A

Type 1 diabetes
DKA
kidney disease

digoxin, insulin (decrease efficacy)

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58
Q

What level is considered as Hypoglycemia?

A

Abnormally low blood glucose level (below 4 mmol/L)

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59
Q

HYPOGLYCEMIA: Mild cases can be treated with ____

Higher intake of ______ and lower intake of ______ to prevent rebound postprandial hypoglycemia

A

diet

high intake of protein and lower carbohydrates

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60
Q

Hypoglycemia Symptoms

Adrenergic: 5

CNS: 8

LATER SIGNS: 4

A

Adrenergic:
Anxiety, tremors, sensation of hunger, PALPITATIONS (fast), sweating

Central nervous system:
Difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness and headache

Later signs:
HYPOTHERMIA (cold), seizures
Coma and death will occur if not treated

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61
Q

Glucagon

Concentrated glucose

IV glucose

Define Diazoxide

A

increase glucose; a natural hormone (can be given by injection)

Rapidly dissolving buccal tablets given and semisolid gels for oral use; better than regular sugar

Intravenous glucose solutions up to 50% D50W (IV from of glucagon)- hospital setting; severe hypoglycemia

Diazoxide: useful for long-term illness such as pancreatic cancer (oral)

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62
Q

Glucagon examples

A

4 glucose tabs

3 pack sugar

8 lifesavers

175ml softdrink

15 ml honey

2.1 mmol/L increase within 20 minutes

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63
Q

Glucose gels

A

must be swallowed; only 1 mmol/L increase at 20 minutes

64
Q

Retest glucose __ minutes after glucose administration

Treat until CBG is above?

A

15 mins

4mmol/L

65
Q

Continuous SC insulin infusion (CSII)

A

type 1 DM

CSII and Basal bolus regimen > intensive diabetes management

continuous delivery of basal insulin- rapid and consistent

achieve glucose and A1C levels that are lower than those with BBR therapy alone> decreases risk for hypoglycemia

66
Q

Basal bolus regimen

insulin type combination?

A

long acting
rapid acting

67
Q

DO not shake NPH insulin instead?

A

roll between hands

do not shake

rotate sites

68
Q

Before giving drugs that alter glucose levels, obtain and document:

A

A thorough history
Vital signs
Blood glucose levels, HbA1c level
Potential complications and drug interactions

69
Q

When to administer insulin?

A

Give if the tray arrives on the unit

70
Q

Before giving drugs that alter glucose levels:

A

Assess the patient’s ability to consume food. (swallowing)

Assess for nausea or vomiting.

Hypoglycemia may be a problem if antidiabetic drugs are given and the patient does not eat.

If a patient is to take nothing by mouth (NPO) for a test or procedure, consult the primary care provider to clarify orders for antidiabetic drug therapy.

71
Q

Overall concerns for any patient with diabetes increase when the patient is at risk for

A

Is under stress
Is pregnant or lactating
Has an infection
Has an illness or trauma

72
Q

Nursing consideration highlights

A

Blood glucose monitoring (CBG & A1C)

Proper injection techniques for insulin or continuous pump therapy (mimics pancreas response to insulin)

Emphasize non-pharm: weight & dietary management, exercise, foot care(damage to BVs/ nerves- PVD, results in loss of sensation, nor enough BF- decreased healing), eye care

Use of medic alert bracelet

Keep a hypoglycemic kit on hand

Oral hypoglycemics may cause photosensitivity

73
Q

A drug that can increase BG?

A

Corticosteroids- suppress the immune system, anti-inflammatory

74
Q

hyperglycemia breath smell

A

acetone smelling breath

75
Q

Thorough patient education is essential regarding:

A

Disease process
Diet and exercise recommendations
Self-administration of insulin or oral drugs
Potential complications

76
Q

When insulin is ordered, ensure:

A

Correct drug
Correct route
Correct type of insulin
Correct dosage

Insulin order and prepared dosages are second-checked with another registered nurse (or per agency policy).

77
Q

When giving insulin

A

Check blood glucose level before giving insulin.

To mix suspensions, roll vials between hands instead of shaking them.

Ensure correct storage of insulin vials.
Only use insulin syringes, calibrated in units, to measure and give insulin.

Ensure correct timing of insulin dose with meals.

Provide thorough patient education regarding self-administration of insulin injections, including timing of doses, monitoring of blood glucose levels, and injection site rotations.

78
Q

Which kind of insulin should you draw up first

A

CLEAR insulin (REGULAR/ RAPID) first then cloudy insulin (INTERMEDIATE)

When drawing up two types of insulin in one syringe, always withdraw the regular or rapid-acting (clear) insulin first.

79
Q

Oral antidiabetic drugs nursing implications

A

Always check blood glucose levels before administering.
Usually given 30 minutes before meals

80
Q

α-Glucosidase inhibitors are given with

A

the first bite of each main meal.

81
Q

Metformin is taken with

Metformin will need to be discontinued if the patient is to undergo studies with________ because of possible renal effects; check with the prescriber.

A

meals to reduce gastrointestinal effects.

contrast dye

82
Q

Nursing Implications

A

Assess for signs of hypoglycemia.

Administer oral form of glucose if the patient is conscious.

Give the patient glucose tablets, liquid, or gel; corn syrup; honey; fruit juice or nondiet soft drink; or have the patient eat a small snack, such as crackers or a half sandwich

83
Q

Deliver ____ or ____ glucagon if the patient is unconscious.

A

Deliver D50W or IV glucagon if the patient is unconscious.

84
Q

Monitor therapeutic response.

A

Decrease in blood glucose levels to the level prescribed by physician

Measure HbA1c to monitor long-term compliance with diet and drug therapy.

Watch for and monitor hypoglycemia and hyperglycemia.

85
Q

Hyperglycemia a fasting glucose of?

non fasting glucose of?

A

7 mmol/L or higher

or non-fasting glucose of 11.1 mmol/L or higher

86
Q

The current key diagnostic criterion for diabetes

glucose level

and A1C level

A

is hyperglycemia with a fasting plasma glucose of higher than
7 mmol/L or a hemoglobin

A1C level greater than or equal to
6.5%.

87
Q

An A1C level of ___% is the threshold for the development
of microvascular disease and a predictor for the development of
macrovascular disease

A

6.5 %

88
Q

Define diabetes and 2 types

A

Often regarded as a syndrome rather than a disease

disorder of carbohydrate metabolism

Type 1 and 2

89
Q

Normal CBG

A

4 to 7 mmol/L as per brenda

4 to 6 in book

90
Q

Pancreas> ductless endocrine

A

secrete hormones into the bloodstream> insulin and glucagon for homeostasis

91
Q

Glucose

A

energy for cells
simplest from of carbs is dextrose

92
Q

Glycogen

A

stored excess glucose in liver, muscles, and adipose

93
Q

Glycogenolysis

A

glycogen in liver converted back to glucose

94
Q

Hormone GLUCAGON

A

released from a-cells of the islet of Langerhans in the pancreas

stimulate glycogen back to glucose

95
Q

INSULIN

created by?

metabolic functions?

what does it store in the liver?

explain fat metabolism

stimulates _____ synthesis

A

from B-cells

metabolic functions: stimulate carbohydrate metabolism (glucose into cells)

In the liver> insulin converts glucose to glycogen

Fat metabolism (lipogenesis > inhibit lipolysis and release of fatty acids from adipose cells)

Stimulate protein synthesis

96
Q

What would happen if there is no INSULIN?

Kidney?

Energy source?

A

Increased PG

Kidneys unable to reabsorb excess glucose and they would excrete large amounts of glucose and ketones into urine

Loss of energy source which leads to polyphagia, weight loss and malnutrition

presence of glucose in kidney > draws large amount of water into urine > osmotic diuresis > leads to polyuria, polydipsia, dehydration

97
Q

polyuria

polydipsia

A

increased urination

increased thirst

98
Q

Hypergycemia

A

excessive concentrations of glucose in the blood

99
Q

Hyperglycemia diagnostic criteria

fasting

A1C

A

fasting- 7 mmol/L or higher

A1C- greater than/ equal to 6.5 %

100
Q

diabetes pathophysiology

A

deficiency of insulin: lack of insulin > destruction of B cells in pancreas> inability to produce insulin

defect in insulin receptors: resistance to insulin

or both

101
Q

2 types of hyperglycemia complications

A

macrovascular- secondary to large vessel damage, caused by deposition of atherosclerotic plaque, impairs central and peripheral

microvascular- secondary to capillary vessels, impairs peripheral circulation

autonomic/ somatic nerve damage- comprised circulation

102
Q

glycoproteins define?

when insulin receptors become defective, they no longer respond to insulin, what happens to glucose?

A

insulin receptors

when insulin receptors become defective, they no longer respond to insulin> and glucose remains in the blood rather than kept in cells

103
Q

Type 1 diabetes

2 effects on insulin

And why?

A

lack of insulin production

OR

production of defective insulin

due to the destruction of B cells (insulin-producing cells)- leads to lack of endogenous insulin by pancreas

104
Q

Type 1 requires ____ for treatment

2 complications

A

needs exogenous insulin to decrease CBG

Complications:

Diabetic ketoacidosis- extreme hyperglycemia, ketones, acidosis, electrolyte imbalance [younger than 65, insulin required]

Hyperosmolar hyperglycemic state- extreme hyperglycemia [34 mmol/L, 65 yr or older, insulin not required in most cases, more than 5 days]

Fewer than 10% of all cases are type 1.

105
Q

DKA

A

elevated glucose and no insulin to allow glucose to be used for energy production= body may break fatty acids for fuel and produce ketones

treatment- fluids, electrolytes, IV therapy

106
Q

Type 2

2 effects on insulin

A

most common; genetic and environmental factors

Caused by insulin deficiency and insulin resistance

insulin resistance; insulin receptors are reduced and has decreased sensitivity to insulin (people can have normal insulin but has high BG)

insulin deficiency (reduced insulin secretion due to loss of normal response of B cells to increased glucose, when B cells do not recognize glucose, they do not secrete insulin > decreased response of insulin receptors

Many tissues are resistant to insulin.
Reduced number of insulin receptors
Insulin receptors less responsive

107
Q

Insulin (hormone) actions in the body 3

A

facilitates the uptake of glucose so it can be used as an energy source

facilitates the transfer of glucose into cells

glucose to glycogen

108
Q

Diabetes symptoms?

fasting glucose of _____
A1C of _____

A

Polyuria
Polydipsia
Polyphagia- excess hunger
Glycosuria
Weight loss
Fatigue
Blurred vision

Elevated fasting blood glucose (higher than 7 mmol/L) or a hemoglobin A1c (HbA1c) level greater than or equal to 6.5%

109
Q

Several comorbid (associated with a disease) conditions

The comorbidities are reffered to as?

A

Obesity
Coronary heart disease
Dyslipidemia- high cholesterolol
Hypertension
Microalbuminemia (protein in the urine)
Increased risk for thrombotic (blood clotting) events

These comorbidities are collectively referred to as metabolic syndrome or cardiometabolic syndrome.

110
Q

Gestational Diabetes

Define

Treatment

A

Hyperglycemia that develops during pregnancy

Insulin must be given to prevent birth defects (Insulin: Prevents hypoglycemia in babies, decreases stillbirth, and weight gain)

Usually subsides after delivery
30% of patients may develop type 2 diabetes within 10 to 15 years.

111
Q

Major Long-Term Complications of Both Types of Diabetes

A

Macrovascular (atherosclerotic plaque)
Coronary arteries
Cerebral arteries
Peripheral vessels

Microvascular (capillary damage)
Retinopathy
Neuropathy
Nephropathy

112
Q

Screening for Diabetes: prediabetes

A1C

FASTING PG

A

HbA1c of 6.0 to 6.4%

Fasting plasma glucose levels higher than or equal to 6.1 mmol/L but less than 6.9 mmol/L

Impaired glucose tolerance test (oral glucose challenge)

113
Q

Screening is recommended every _ ____ for all patients 40 years of age and older

A

Screening is recommended every 3 years for all patients 40 years of age and older

114
Q

Nonpharmacological Treatment Interventions

A

Type 1: Always requires insulin therapy

Type 2
Weight loss
Improved dietary habits
Smoking cessation
Reduced alcohol consumption
Regular physical exercise

115
Q

Glycemic Goal of Treatment

A1C

FASTING PG

2 HOURS POSTPRANDIAL TARGET

A

HbA1c of less than 7%

Fasting blood glucose goal for diabetic patients: 4 to 7 mmol/L

2-hour postprandial target of 5 to 10 mmol/L

116
Q

Treatment for Diabetes

TYPE 1

TYPE 2

A

Type 1
Insulin therapy

Type 2
Lifestyle changes
Oral drug therapy
Insulin when the above no longer provide glycemic control

117
Q

Types of Antidiabetic Drugs

A

Insulins

Oral hypoglycemic drugs

A combination of oral antihypoglycemic and insulin controls glucose levels.
Some new injectable hypoglycemic drugs may be used in addition to insulin or antidiabetic drugs.

118
Q

A1C IS AN INDICATOR OF

A

indicator of glycemic control 2 to 3 months (lifespan of RBC)

119
Q

A1C for very sick patients

A

7 to 8.5 %

120
Q

Insulins function as a substitute for?

effects are the same as those normal?

synthesized in labs using

A

Function as a substitute for the endogenous hormone

Effects are the same as those of normal endogenous insulin

RDNA technology

121
Q

Insulin restores the diabetic patient’s ability to:

A

Metabolize carbohydrates, fats, and proteins

Store glucose in the liver

Convert glycogen to fat stores

122
Q

Four Major Classes of Insulins and their examples

A

Rapid Acting (insulin lispro)

Short Acting (regular insulin)

Intermediate Acting (insulin NPH)

Long Acting (insulin detemir and glargine)

123
Q

Human insulin

derived using?

recombinant insulin produced by?

goal (2)

A

Derived using recombinant deoxyribonucleic acid (DNA) technologies

Recombinant insulin produced by bacteria and yeast

Goal: tight glucose control
To reduce the incidence of long-term complications
Individualized dose

124
Q

exogenous insulin:

A

substitute for endogenous
replace insulin
restore ability to metabolize carbs, fats and protein
does not reverse damage to receptors

125
Q

Rapid-acting treatment for types 1 and 2 diabetes

Onset

Peak

Duration

When to give?

2 names of medications

Can it be given via CSIP? what about via IV?

A

Most rapid onset of action (10 to 15 minutes)

Peak: 1 to 2 hours

Duration: 3 to 5 hours (shorter duration)

Patient must eat a meal after injection

Insulin lispro (Humalog®)
~~~~Action similar to that of endogenous insulin
Insulin aspart (NovoRapid®)/ Insulin glulisine (Apidra®)

May be given subcutaneously or via continuous subcutaneous infusion pump (but not intravenously)

126
Q

Insulin lispro

A

facilitates uptake of excess glucose at hepatic insulin receptor sites for storage in liver as glycogen

facilitates glucose to glycogen in liver

127
Q

RAPID ACTING- given when?

A

eat a meal after injection of rapid acting

128
Q

Short-Acting Insulins

Onset

Peak

Duration

When to give?

2 names of medications

Can it be given via IV?

A

Regular insulin (Humulin R®, Novolin ge Toronto®)

Routes of administration: intravenous (IV) bolus, IV infusion, intramuscular, subcutaneous

Onset (subcutaneous route): 30 minutes

Peak (subcutaneous route): 2 to 3 hours

Duration (subcutaneous route): 6.5 hours

for DKA/ COMA

129
Q

Intermediate-Acting Insulins

names

apperance

O

P

D

A

Insulin isophane suspension (also called NPH), Humulin N, NovoliN ge NPH

CLOUDY appearance

Often combined with regular insulin

Onset: 1 to 3 hours

Peak: 5 to 8 hours

Duration: up to 18 hours

130
Q

What is often combined with Intermediate-Acting Insulins?

A

Regular insulin (short-acting)

131
Q

Intermediate-Acting Insulins ONSET AND DURATION

A

slower onset and longer duration

132
Q

Long-Acting Insulins

Onset

Peak

Duration

CAN BE DOSED….

2 names of medications

provides

A

Insulin glargine (Lantus®) & Detemir

Clear, colourless solution

Constant level of insulin in the body

Usually dosed once daily

Can be dosed every 12 hours

Referred to as basal insulin

Onset: 90 minutes

Peak: none

Duration: 24 hours

133
Q

Bolus insulin

A

rapid-acting
short -acting

treats at time of meals

134
Q

Basal insulin

A

intermediate- acting
long-acting

fasting periods and in between meals

135
Q

Insulin detemir duration of action and effect on frequency

A

Insulin detemir

Duration of action is dose-dependent.
Lower doses require twice-daily dosing.
Higher doses may be given once daily.

136
Q

Long acting insulin

provides a ____ level of insulin

referred to as

A

Provides a constant level of insulin

referred to as basal insulin

137
Q

Fixed-Combination Insulins

A

Fixed combinations
Humulin 30/70
Novolin 30/70, 40/60, 50/50
NovoMix® 30
Humalog Mix25®
Humalog Mix50®

138
Q

Each contains two different insulins, fixed combinations: What are the two?

A

One intermediate-acting type

Either one rapid-acting type (Humalog, NovoLog) or one short-acting type (Humulin)

intermediate + (rapid or short)

139
Q

Insulin contraindicated for drug allergy

A

*patients with dietary restrictions to pork products

140
Q

Insulin adverse effects

A

Hypoglycemia
Tachycardia, palpitations
Headache, lethargy, tremors
Blurred vision, dry mouth, hunger

141
Q

Insulin interactions

What drugs cause? >Reduced effects which result in elevated blood glucose: 5

Increased effects resulting in lowered blood glucose: 7

A

Β blockers, corticosteroids, epinephrine, furosemide, thyroid hormones

Alcohol, anabolic steroids, sulfa drugs, ACE inhibitors, MAOIs, propanolol and salicylates

142
Q

Special Considerations

A

Hospitalized patients may be put on a ‘sliding scale’ protocol to try and achieve better glycemic control (not preferred)

Some controversy to this but some conditions or NPO status or TPN alters the maintenance normalcy for patients as compared to home

143
Q

__________ has been proven to be more effective

A

Basal bolus strategy

144
Q

Sliding-Scale Insulin Dosing
* type of insulins
* used for which patients
* relationship to glucose levels

A

Subcutaneous rapid-acting (lispro or aspart) or short-acting (regular) insulins are adjusted according to blood glucose test results.

Typically used in hospitalized diabetic patients or those on total parenteral nutrition or enteral tube feedings

Subcutaneous insulin is ordered in an amount that increases as the blood glucose increases.

Recent research does not support sliding-scale use; nonetheless, sliding scale is still commonly used.

145
Q

Disadvantage of Sliding-Scale Insulin Dosing

A

Delays insulin administration until hyperglycemia occurs, resulting in large swings in glucose control.

146
Q

Basal-Bolus Insulin Dosing
* types of insulin
* describe what it does

A

Preferred method of treatment for hospitalized patients with diabetes

Mimics a healthy pancreas by delivering basal insulin constantly as a basal and then as needed as a bolus

Basal insulin is a long-acting insulin (insulin glargine).

Bolus insulin (insulin lispro or insulin aspart [rapid acting] )

147
Q

Special Considerations

A

Be aware of special dosing guidelines for children

Insulin therapy is the only currently recommended drug therapy for pregnant women

Reduce risk of congenital anomalies, stillbirth~~~Helps with milk production (hyperglycemia impedes this)

148
Q

Other Injectable Antidiabetic Drugs

A

Amylin agonist
pramlintide (Symlin®)

Incretin mimetics
exenatide (Byetta®)
liraglutide (Victoza®)

149
Q

Amylin agonist

A

Mimics hormone amylin

Slows gastric emptying

Suppresses glucagon secretion, reducing hepatic glucose output

Used when other drugs have not achieved adequate glucose control

Subcutaneous injection

150
Q

Incretin mimetic

action?

used only in?

A

Mimics the incretin hormones

Enhances insulin secretion from β cells of the pancreas

Used only for type 2 diabetes

Exenatide: injection pen device

151
Q

Injectable Antidiabetic Drugs: Adverse Effects

A

Amylin agonist
Nausea, vomiting, anorexia, headache

Incretin mimetics
Nausea, vomiting, and diarrhea
Rare cases of hemorrhagic or necrotizing pancreatitis
Weight loss

152
Q

a- glucosidase inhibitor

  • mechanism of action
  • a glucosidase enzyme function
  • important FACT
A

inhibits a-glucosidase enzymes > which delays glucose absorption

a glucosidase enzyme> responsible for the hydrolysis of oligosaccharides and disaccharides into glucose

must be taken with food > first bite of a meal, so that post-prandial elevation can be prevented.

153
Q

a glucosidase inhibitor 1 drug

A

acarbose (less commonly used)

154
Q

a- glucosidase

interactions

contraindications

A

interactions- digoxin, ranitidine, propanolol

contraindication: IBS, malabsorption, intestinal obstruction

155
Q

a glucosidase indication

A

indication- controlling elevated postprandial glucose levels

156
Q

a-glucosidase AE

A

AE: GI effects- flatulence, diarrhea, abd pain