Alcohol Withdrawal and Diabetes Mellitus - PowerPoint Presentation

Slide1

Alcohol Withdrawal and Diabetes Mellitus ManagementOctober 20, 2014

Jennifer Bauman, RN, BA, PCCN

PhD Student

The Ohio State University College of Nursing

Nursing 6270

Autumn 2014

Slide2

Objectives

Define alcohol withdrawal.

Discuss the CIWA scale.

Describe nursing management of inpatient alcohol withdrawal.

Define diabetes mellitus.

Discuss nursing considerations for the hospitalized patient with diabetes mellitus.

Describe medical and lifestyle (i.e., outpatient) management of diabetes mellitus.

Slide3

Prevalence and Definition

Estimated 8 million alcohol dependent individuals in the U.S.

500,000 episodes of alcohol withdrawal require pharmacological intervention

Alcohol use disorder (DSM-V)

As of September 17, 10/33 patients on 8PCU had a primary/admitting diagnosis of drug or alcohol intoxication/withdrawal (unknown number of patients had it listed as a secondary diagnosis)

Estimated 15-20% of hospitalized patients afflicted by alcohol use disorder

(

Kosten

et al., 2003)

Slide4

DSM-V Diagnostic Criteria for Alcohol Use Disorder

A

problematic pattern of alcohol use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month

period:

Alcohol is often taken in larger amounts or over a longer period than was intended.

There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.

A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects.

Craving, or a strong desire or urge to use alcohol.

Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home.

Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol.

Important social, occupational, or recreational activities are given up or reduced because of alcohol use.

Recurrent alcohol use in situations in which it is physically hazardous.

Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol.

Tolerance, as defined by either of the following:

A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.

A markedly diminished effect with continued use of the same amount of alcohol.

Withdrawal, as manifested by either of the following:

The characteristic withdrawal syndrome for alcohol (refer to Criteria A and B of the criteria set for alcohol withdrawal).

Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.

Slide5

Specify if: In early remission: After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use alcohol,” may be met).In sustained remission: After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use alcohol,” may be met).Specify if: In a controlled environment: This additional specifier is used if the individual is in an environment where access to alcohol is restricted

(cont’d)

DSM-V Diagnostic Criteria for

Alcohol Use Disorder

Slide6

Common, Fatal, Costly Problem

Alcohol Use Disorders (AUDs) in the United States:

Adults (ages 18+): 

Approximately 17 million adults ages 18 and older (7.2 percent of this age group) had an AUD in 2012. This includes 11.2 million men (9.9 percent of men in this age group) and 5.7 million women (4.6 percent of women in this age group).

3

Youth (ages 12–17):

 In 2012, an estimated 855,000 adolescents ages 12–17 (3.4 percent of this age group) had an AUD. This number includes 444,000 females (3.6 percent) and 411,000 males (3.2 percent).

5

 

Alcohol-Related Deaths:

Nearly 88,000

7

 people (approximately 62,000 men and 26,000 women

8

) die from alcohol related causes annually, making it the third leading preventable cause of death in the United States.

7

In 2012, alcohol-impaired-driving fatalities accounted for 10,322 deaths (31 percent of overall driving fatalities).

9

 

Slide7

Economic Burden:In 2006, alcohol misuse problems cost the United States $223.5 billion.10Almost three-quarters of the total cost of alcohol misuse is related to binge drinking.10Global Burden:In 2012, 3.3 million deaths, or 5.9 percent of all global deaths (7.6 percent for men and 4 percent for women), were attributable to alcohol consumption.11Alcohol contributes to over 200 diseases and injury-related health conditions, most notably alcohol dependence, liver cirrhosis, cancers, and injuries.12 In 2012, alcohol accounted for 5.1 percent of disability adjusted life years (DALYs) worldwide.11Globally, alcohol misuse is the fifth leading risk factor for premature death and disability; among people between the ages of 15 and 49, it is the first.13Family Consequences:More than 10 percent of U.S. children live with a parent with alcohol problems, according to a 2012 study.14 

Common, Fatal, Costly Problem

Slide8

(Ethyl) Alcohol = Ethanol

Ethyl alcohol is the only type of consumable ethanol.

Central

nervous system

(CNS) depressant

Simultaneously

enhances inhibitory tone

via

modulation of gamma-

aminobutyric

acid (GABA) activity

and

dampens

excitatory tone

via

modulation of excitatory amino acid

activity

To keep the inhibitory and excitatory tones balanced (i.e., homeostasis), must have constant presence of ethanol.

Abrupt cessation of ethanol creates an imbalance (i.e., interrupts homeostasis) =

overactivity

of CNS

Slide9

Slide10

Neurotransmitters Affected

Remember that ethanol enhances inhibitory and dampens excitatory tones, resulting in CNS depression.

GABA:

major

inhibitory

neurotransmitter with very specific binding sites for ethanol.

Chronic ethanol use = insensitivity to GABA

More inhibitor is needed to maintain constant inhibitory tone = tolerance to large doses (think of the “functioning” alcoholic)

Glutamate

:

one of the major

e

xcitatory

amino acids

When

glutamate binds to the N-methyl-D-aspartate (NMDA) receptor, calcium influx leads to neuronal excitation.

Ethanol dampens glutamate

induced

excitation.

Increasing sensitivity to glutamate = adaption, with the goal to

maintain a normal state of

arousal

Slide11

Long term effects of Alcohol Misuse

Liver disease

Cirrhosis

“Among

all cirrhosis deaths in 2009, 48.2 percent were alcohol related. The proportion of alcohol-related cirrhosis was highest (70.6 percent) among decedents ages

35–44”(NIAAA, 2014).

However, only 5-10% of alcoholics develop cirrhosis

Fatty liver disease

Hepatitis

1 in 3 liver transplants in 2009 were due to alcohol-related disease (NIAAA, 2014)

Increased risk for cancer of

mouth, esophagus, pharynx, larynx, liver, and

breast

Pancreatitis

Malnutrition

Wernicke’s Encephalopathy

Higher risk for injury, especially falls

Impaired judgment = high risk behavior = increased risk for STIs, sexual assault, etc.

Slide12

Alcohol Withdrawal

(If it doesn’t work, use

this link

:

http://www.youtube.com/watch?v=bAEcA4mCMfc)

Slide13

DSM-V Diagnostic Criteria for Alcohol Withdrawal

Cessation

of (or reduction in) alcohol use that has been heavy and prolonged.

Two (or more) of the following, developing within several hours to a few days after the cessation of (or reduction in) alcohol use described in Criterion A:

Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).

Increased hand tremor.

Insomnia.

Nausea or vomiting.

Transient visual, tactile, or auditory hallucinations or illusions.

Psychomotor agitation.

Anxiety.

Generalized tonic-

clonic

seizures

.

Slide14

The signs or symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance.Specify if: With perceptual disturbances: This specifier applies in the rare instance when hallucinations (usually visual or tactile) occur with intact reality testing, or auditory, visual, or tactile illusions occur in the absence of a delirium.

DSM-V Diagnostic Criteria for Alcohol Withdrawal

Slide15

Symptoms of Withdrawal

Insomnia

Anxiety and/or Fear

Restlessness

Nausea and/or Vomiting

Headache

Seizures – may need CT scan, lumbar puncture

Altered Sensory Perceptions, including visual (common), tactile (common), auditory

Tremors

Diaphoresis

Tachycardia, which may/may not be accompanied by palpitations (why??)

Slide16

Slide17

Delirium Tremens (DT)

“… hallucinations

, disorientation, tachycardia, hypertension, fever, agitation, and diaphoresis in the setting of acute reduction or abstinence from

alcohol.”

Last up to 7 days, mortality rate of 5%

Increased cardiac

indices, oxygen delivery, and oxygen

consumption

Arterial

pH rises

due

to

hyperventilation

(respiratory alkalosis)

= decrease

in cerebral blood flow

F

luid

and electrolyte

status:

Hypovolemic r/t diaphoresis

, hyperthermia, vomiting, and

tachypnea

Hypokalemia r/t

renal and

extrarenal

losses, alterations in aldosterone levels, and changes in potassium distribution across the cell

membrane

Hypomagnesemia

r/t malnutrition; may

predispose to dysrhythmia

(

torsades

des pointes) and seizures

Hypophosphatemia r/t malnutrition; may

contribute to cardiac failure and

rhabdomyolysis

.

Slide18

Who is at risk for DT?

A

history of sustained drinking

A history of previous DT

Over age 30

The presence of a concurrent illness

The presence of significant alcohol withdrawal in the presence of an elevated alcohol level

A longer period since the last drink (

ie

, patients who present with alcohol withdrawal more than two days after their last drink are more likely to experience DT than those who present within two days

)

Slide19

Other diagnoses to consider

“A premature diagnosis of alcohol withdrawal can lead to inappropriate use of sedatives, which can further delay accurate diagnosis

.”

Infection

(

e.g.,

meningitis

)

Trauma

(

e.g.,

intracranial hemorrhage

)

Metabolic derangements

Drug overdose

H

epatic failure

Gastrointestinal bleeding

Slide20

Nursing Management: ADPIE

Assessment

Diagnosis

Plan and Goals of Care

Implementation

Evaluation

Slide21

Assessment: Clinical Institute Withdrawal Assessment (CIWA)

Slide22

Assessment: CIWA Calculation

http://www.mdcalc.com/ciwa-ar-for-alcohol-withdrawal/

Slide23

Assessment – beyond CIWA

Questions to ask:

CAGE questions

(

Kosten

et al, 2003)

Can you

cut

down on your drinking?

Are you

annoyed

when asked to stop drinking?

Do you feel

guilty

about your drinking?

Do you need an

eye opener

drink in the morning when you wake up?

How long have you gone without alcohol in the past six months?

Has anyone ever advised that you cut down on your drinking?

When was the last drink (i.e., the most recent alcohol consumption)?

How much alcohol per day?

How long has the patient been dependent on alcohol?

Has he/she ever experienced withdrawal or delirium tremens before?

If so, how many times has this occurred, and did he/she ever have seizures?

Slide24

Continued assessment …

Vital signs – what would you expect to find, and why?

See “Symptoms” slide for signs/symptoms of withdrawal

Risk for elopement, falls, aspiration

Smoking status

Blood sugar –

Accu

check

Urine drug/toxicity screen

Blood work to collect:

Chemistry

Complete Blood Count (CBC) with differential and platelet

Coagulation panel (PT, INR, PTT)

Liver Function Tests (LFT)

Uric acid

Alcohol, whole blood

Drug/toxicity screen – should be collected at the same time as the urine, if possible

Slide25

Diagnosis

Risk for Injury (especially

falls

!) r/t alcohol withdrawal

Risk for Elopement r/t alcohol withdrawal

Risk for Sensory-Perceptual Alterations r/t alcohol withdrawal

Anxiety and/or Fear r/t alcohol withdrawal

aeb

restlessness, tachycardia, hypertension

Risk for Aspiration (Ineffective Breathing Pattern) r/t alcohol withdrawal

Risk for Seizures r/t alcohol withdrawal

Slide26

Plan and Goals of Care

The patient will remain free from falls during the hospital stay by using bed exit alarm and frequent monitoring by staff.

The patient will not elope from the hospital during his/her stay through frequent monitoring, purple gown, security alert.

The patient will not aspirate during his/her stay by keeping HOB > 30 degrees, monitoring during PO intake, staff evaluation for safe swallow.

Slide27

Interventions

IV access

Administer medications (as ordered by LIP)

Possible sitter/safety coach and/or to be closer to nurses’ station

If at risk for elopement, place in special gown (at OSUWMC, it is bright purple), notify security of increased risk, and keep close to nurses’ station, away from elevators.

Going off the unit is contraindicated, both due to risk for elopement and medication administration

Avoid the use of restraints, especially LBB

Slide28

Interventions

Bed exit alarm

Seizure pads on bedrails

HOB at 30 degrees or greater, if no contraindications

Quiet, dark, calm environment

Fan or cool washcloths

Nurse should present calm demeanor

Limit setting

Nicotine replacement

Consults: social work, nutrition, psychiatry, nicotine dependence

Slide29

Interventions: Medications

Chlordiazepoxide

(Librium)

– long-acting benzodiazepine

Diazepam (Valium)

– long-acting

benzo

Lorazepam (Ativan)

– short-acting

benzo

Flumazenil (

Romazicon

)

– reversal agent for

benzo

Clonidine (

Catapres

)

-

centrally acting alpha-2

agonist, for severe DT, but may mask symptoms of worsening status

Phenobarital

– anticonvulsant, if severe DT or status

epilecticus

AVOID

the routine

use of anticonvulsants, beta blockers (mask symptoms) and antipsychotics (lower the seizure threshold)

Vitamins

, especially folic acid and thiamine

Electrolytes

, especially glucose, magnesium, phosphate, and potassium

Intravenous fluids

, if not contraindicated

Slide30

Interventions: Medications used at OSUWMC

Slide31

Evaluation

Back to assessment – check CIWA score per the protocol Re-assess

Slide32

Questions?

Slide33

References

American Psychiatric Association. (2013).

Diagnostic and statistical manual of mental

disorders

(5th ed.). Arlington, VA: American Psychiatric Publishing. Retrieved September 30, 2014, from http://dsm.psychiatryonline.org/book.aspx?bookid=556.

Hoffman, R.S., &

Weinhouse

, G.L. (2013). Management of moderate and severe alcohol withdrawal syndromes. In S.J.

Traub

& J.

Grayzel

(Eds.), 

UpToDate

. Retrieved from http://www.uptodate.com/.

Kosten

, T.R., & O’Connor, P.G. (2003). Management of drug and alcohol withdrawal.

New England Journal of Medicine, 348

(18), 1786-95.

MDCalc

. (2014). CIWA-

Ar

for Alcohol Withdrawal. Retrieved September 20, 2014, from http://www.mdcalc.com/ciwa-ar-for-alcohol-withdrawal.

National Institute on Alcohol Abuse and Alcoholism (NIAAA). (2014). Alcohol facts and statistics.

Alcohol and Your Health.

Retrieved September 30, 2014, from http://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-facts-and-statistics.

National

Institute on Alcohol Abuse and Alcoholism. (

n.d.

). What is a standard drink?.

Alcohol and Your Health

. Retrieved September 30, 2014, from

http://

www.niaaa.nih.gov/alcohol-your-health/overview-alcohol-consumption/standard-drink

.

Nurselabs.com (

n.d.

). 5 Alcohol Withdrawal Nursing Care Plans. Retrieved September 30, 2014, from

http

://nurseslabs.com/5-alcohol-withdrawal-nursing-care-plans

/

.

Office

of Women’s Health at the U.S. Department of Health and Human Services. (2013). Straight talk about alcohol.

GirlsHealth.gov.

Retrieved September 30, 2014, from www.girlshealth.gov.

Weed

, H.G. (2011).

Clinician’s Guide to Alcohol Withdrawal as a Secondary Diagnosis

. 2

nd

Edition. From The Ohio State University Medical Center Evidence Based Practice Clinical Resources. Retrieved September 20, 2014, from http://www.osumc.edu.

Slide34

TAKE A BREAK (please)!

Slide35

Diabetes

Slide36

Slide37

Diabetes: A huge public health problem

Diabetes affects

29.1

million

people of all

ages

Diagnosed: 21 million

Undiagnosed: 8.1 million

That’s

9.3

%

of the U.S.

population!

About

1.7

million

adults were

newly diagnosed

with diabetes in

2012

in the U.S.

An estimated

86

million

American adults have

pre-diabetes

By 2050,

1 in 3

Americans will have diabetes!

Slide38

Slide39

Why individuals with diabetes should be concern

Medical expenses

for people with diabetes are more than

2 times higher

than for people without diabetes.

The total annual

cost

of diabetes is

$245 billion

(CDC, 2014)

Direct medical: $176 billion

Indirect: $

6

9 billion

“In

2003–2006, after adjusting for population age differences, rates of death from all causes were about

1.5 times higher

among adults aged 18 years or older with diagnosed diabetes than among adults without diagnosed

diabetes” (CDC, 2014).

INEQUALITIES – those in lower socioeconomic position and non-whites are more likely to develop T2DM

Slide40

Diabetes Mellitus

Definition

“Diabetes

is a group

of metabolic

diseases characterized by

hyperglycemia resulting

from defects in

insulin secretion

, insulin action, or

both” (ADA, 2010, S62).

“Deficient insulin action

results from inadequate insulin

secretion and/or

diminished tissue

responses to

insulin at one or more points

in the

complex pathways of hormone

action” (ADA, 2010, S62).

Classifications

Prediabetes

Type 1 Diabetes Mellitus (T1DM)

Type 2 Diabetes Mellitus (T2DM)

Gestational Diabetes Mellitus

Monogenic Diabetes Mellitus

Other causes: surgery, medications, pancreatic disease

Slide41

Slide42

https://www.youtube.com/watch?v=pQjWgOSFChI

Diabetes complications

Slide43

Diabetes is risky business for your heart

Overall, the

risk for death

among people with diabetes is about

twice

that of people without diabetes.

Poorly controlled

diabetes is the

7th

leading

cause of death

in the United States.

Adults with diabetes have

heart disease death

rates about

2 to 4 times higher

than adults without diabetes.

The

risk for stroke

is

2 to 4 times higher

among people with diabetes.

Slide44

… and for your eyes, kidneys, nerves, mouth, and mental health …

Poorly controlled

diabetes is the leading cause of

kidney failure

, non-traumatic lower-limb

amputations

, and new cases of

blindness

among adults in the United States

.

Those with diabetes have about

twice the risk of gum disease

than those without diabetes.

People with diabetes are

more susceptible

to many other illnesses.

People with diabetes are

twice

as likely to have

depression.

Slide45

True or False?

Diabetes

is the leading cause of blindness, amputations, and kidney problems.

Slide46

How to prevent complications

Proper

glycemic control can prevent or delay the micro- and macro-vascular complications that lead to poor outcomes (DCCT, 1993; Stratton et al.,

2000).

This can

be achieved through adequate self-management (SM) (

Atak

et al., 2008; Chen et al., 2013;

Aljasem

et al., 2001; Osborn,

Bains

, &

Egede

, 2010).

Regular follow-up with primary care providers is ESSENTIAL.

Slide47

Diabetes overview

https://www.youtube.com/watch?v=MGL6km1NBWE

Slide48

Pathophysiology Overview

The pancreas

produces insulin in response to an increase in blood sugar, which occurs after eating

food

Insulin

functions as the “key” to let the sugar into the cells. Without the insulin, the sugar remains in the blood and cannot be used by the cell for daily functions.

For

those with Type 1 diabetes, the pancreas is unable to make insulin.

For

those with Type 2 diabetes, the cells have difficulty using the insulin, which happens when the cells become resistant to the insulin.

After a while, the pancreas gets “tired” and produces less insulin.

Both

result in high blood sugar levels, which leaves the cells starved of sugar.

Slide49

Glucose Regulation

Glucose = major energy source

BG level “regulated by rate of

consumption and intestinal absorption of dietary carbohydrate, the rate

of utilization

of glucose by peripheral tissues and the loss of glucose through

the kidney

tubule, and the rate of removal or release of glucose by the

liver” (

Nordlie

et al., 1999, p. 380).

Liver regulates BG level through

the following:

Glycogenesis

:

uptake

of

extra glucose

, to store as

glycogen

Glycogenolysis

:

release of glucose by turning glycogen into glucose

Gluconeogenesis

:

release of glucose by harvesting amino acids, waste products, fat byproducts

Ketogenesis

:

when glycogen and insulin levels are low, the liver breaks down fats into ketones to use as energy for less essential organs, reserving glucose for brain, RBCs, some of the kidneys

(REMEMBER THIS FOR LATER!)

Slide50

Slide51

Slide52

Slide53

Insulin

Discovered in 1922 by

Banting

and Best (

Saltiel

, 2000

)

Anabolic (i.e., storage) hormone

Essential

for appropriate tissue development, growth, and maintenance of whole-body glucose

homeostasis

S

ecreted

by the

β cells of the pancreatic islets of Langerhans

in response to increased circulating levels of glucose and amino acids

(after

a

meal)

Regulates glucose

homeostasis

(i.e., balance) at

many sites, reducing hepatic glucose output (via decreased gluconeogenesis and

glycogenolysis

)

Increases the

rate of glucose uptake, primarily into striated muscle and adipose

tissue

Affects

lipid

metabolism by increasing

lipid synthesis in liver and fat

cells and enhancing

fatty acid release from triglycerides in fat and

muscle

Acts as the “key” to let glucose into the cells, via an insulin receptor on the outside of the cell (extracellular)

Slide54

Insulin Functions

Slide55

Slide56

Pre-Diabetes and Metabolic Syndrome

Metabolic Syndrome (AHA, 2014)

Affects approximately 1/3 of Americans

Increased risk for diabetes, stroke, heart disease

3 of 5 criteria

Fasting BG greater than 100 mg/

dL

Waist circumference greater than 35 inches for women, 40 inches for men (central obesity, indicating increased visceral adipose tissue)

Hypertension (BP >130/85)

Triglyceride level greater than 150mg/

dL

HDL less than 50mg/

dL

for women, 40mg/

dL

for men

Pre-diabetes (CDC, 2014; ADA, 2012)

15-30% of those with

prediabetes

will develop T2DM in 5 years

Elevated fasting BG (>100 -125 mg/

dL

) on two occasions

Oral glucose tolerance test of 140-199mg/

dL

HbA1c 5.7-6.4

%

Slide57

Slide58

Treatment of Prediabetes and Metabolic Syndrome

LOSE WEIGHT

Physical activity >150 minutes/week

Dietary considerations

Control BP, lipids, cholesterol levels

Diabetes Prevention Program (DPP)

Slide59

Slide60

Type 1 Diabetes

INSULIN DEPENDENT – no insulin is made by the pancreas

5-10% of total diabetes cases

Genetic predisposition and environmental factors

Autoimmune destruction of insulin-producing beta cells

Also at risk for other autoimmune diseases, such as Graves’, Hashimoto’s, Addison’s, vitiligo, celiac

sprue

, autoimmune hepatitis, myasthenia gravis, pernicious anemia (ADA, 2010).

Minority do not exhibit autoimmune destruction = idiopathic

50-75% of cases diagnosed in childhood or adolescence

25-50% diagnosed in adulthood

Latent Autoimmune Disease of Adults (LADA)

Many misdiagnosed as type 2 diabetes (T2DM)

For LADA, typically only 1 antibody present (often GADA)

Slide61

T1DM Testing

Hemoglobin A1C

=

glycated

hemoglobin = average BG over the past 8-12 weeks (lifespan of RBC)

Can

usually be confirmed by islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA), insulin antibodies (IAA), and/or insulinoma-2–associated antibodies (IA-2A) (ADA, 2010;

Lightsey

, 2011

)

85-90% of patients have these antibodies (ADA, 2010)

Genetics: strong HLA

(human leukocyte antigen) associations

, with linkage to the DQA and DQB genes, and it is influenced by the DRB genes (ADA, 2010)

C-peptide level low – positive relationship to insulin (linked when

proinsulin

made by pancreas) – examines how much insulin the pancreas is producing

Oral glucose tolerance test >200mg/

dL

Fasting BG > 126mg/

dL

For T1DM and T2DM: HbA1C >6.5% (some organizations state >7% -

most say >6.5%

)

Slide62

Risk Factors/Demographics

Onset at any age, but most are diagnosed when under age 30

Certain HLA types = 3-5x higher risk of T1DM (

Pellico

, 2013)

Genetic predisposition PLUS environmental factors

More

than 15,000 children and 15,000 adults—approximately 80 people per day—are diagnosed with

T1DM

in the

U.S. annually (JDRF)

85%

of people living with

T1DM

are adults, and

15% children (JDRF)

The

prevalence of

T1DM

in Americans under age 20 rose by 23 percent between 2001 and

2009 (JDRF)

The

rate of

T1DM

incidence among children under age 14 is estimated to increase by

3% annually worldwide (JDRF).

Slide63

Slide64

T1DM Presenting Symptoms

DEHYDRATION

Hyperglycemia

Polydypsia

Polyuria

Polyphagia

Glycosuria (if above renal reabsorption threshold of 180-200mg/

dL

)

Blurred vision

Weight loss

Impaired growth

Decreased immunity

Diabetic Ketoacidosis (DKA)

EVERYONE PRESENTS DIFFERENTLY –

depends on how much beta cell function remains

Slide65

T1DM Treatment

New therapies: Vc-01 (beta cell encapsulation), islet cell transplant

Medications: Insulin

(discussed later in the presentation)

Monitor

blood

sugars

Maintain your blood glucose within normal limits, usually

70-130 before meals

and

less than 180 1-2 hours after meals

.

Keep your Hemoglobin A1C (

Hgb

A1C)

below 7

. (

Hgb

A1C is a blood test that shows what your blood glucose control has been over 2-3 months.)

Lifestyle management

Reduce carbohydrate intake, especially simple carbohydrates (i.e., anything that ends in an “–

ose

”) … High-fiber, low glycemic index foods are best

Physical activity >150 minutes/week

Weight management

Mental health considerations

Slide66

Type 2 Diabetes (T2DM)

NON-INSULIN DEPENDENT

Obesity, sedentary lifestyle, aging, genetic predisposition

Increased insulin resistance

 Relative insulin deficiency (i.e., insulin supply is less than the demand)

Resistance = “state

of reduced responsiveness to normal circulating concentrations of

insulin” (

Saltiel

, 2000).

Pancreas compensates for insulin resistance by producing more insulin (

hyperinsulinemia

). After a while, the beta cells can no longer compensate, creating glucose

intolerance and hyperglycemia.

Hyperglycemia for many years prior to diagnosis = increased risk of micro- and macro-vascular complication development

Slide67

Slide68

T2DM Testing

C-peptide level

moderate to high

–

positive correlation with insulin

Oral glucose tolerance test >200mg/

dL

Fasting BG > 126mg/

dL

HbA1C >6.5% (some organizations state >7% -

most say >6.5%)

Slide69

Risk Factors/Demographics

Obesity (especially visceral/trunk) – BMI

>

25 kg/m

2

Poor dietary habits

Men slightly more than women

Sedentary lifestyle/physical

inactivity

Older age (

>

45

y.o

.)

Family

history of

diabetes

If either parent suffers from

T2DM, a

child’s risk of developing the disease is almost

15%

  If both parents have the condition, the risk of developing it is

75%.

History

of gestational

diabetes or baby over 9lbs (10% of those with GD develop T2DM immediately; 35-60% within 10-20 years)

Slide70

Risk Factors/Demographics

Impaired glucose metabolism

HDL cholesterol

<

35mg/

dL

and/or triglyceride level

>

250mg/

dL

Insulin resistance and

hyperinsulinemia

Race/ethnicity

Increased risk for African Americans, Hispanics/Latinos, American Indians (e.g., Pima Indians), some Asians, and Native Hawaiians or other Pacific Islanders

Asian Americans have a 9% higher risk of diabetes. Hispanics have a 12.8% higher risk, and non-Hispanic blacks have a 13.2% higher risk of diabetes than non-Hispanic white adults in the U.S.

In children and adolescents, diagnosed more frequently among American Indians, African Americans, Hispanics/Latinos, Asians, and Pacific Islanders

Slide71

Slide72

T2DM Presenting Symptoms

Slow progression of glucose intolerance, so minimal to no symptoms (usually)

May include

Irritability

Fatigue

Polydipsia

Polyuria

Polyphagia (sometimes)

Poor wound healing

Frequent infections

Vision changes

Slide73

T2DM Treatment

Medications: oral agents, then insulin in later stages

(we’ll speak more about this later)

Monitor blood

sugars

Maintain your blood glucose within normal limits, usually

70-130 before meals

and

less than 180 1-2 hours after meals

.

Keep your Hemoglobin A1C (

Hgb

A1C)

below 7

. (

Hgb

A1C is a blood test that shows what your blood glucose control has been over 2-3 months.)

Lifestyle management

Reduce carbohydrate intake, especially simple carbohydrates (i.e., anything that ends in an “–

ose

”) …

High-fiber, low glycemic index foods are best

Physical activity >150 minutes/week

Weight management – lose 5-10% of body weight

Mental health considerations

Slide74

Gestational Diabetes Mellitus (GDM)

A form

of glucose intolerance diagnosed during the second or third trimester of pregnancy.

Placental hormones cause hyperglycemia and insulin resistance.

In up to 14% of pregnancies (

Pellico

, 2013, p. 820).

Usually glucose tolerance testing at 24-28 weeks, but do earlier if at increased risk.

The risk factors for

GDM are

similar to those for

T2DM.

Within 1 year after

pregnancy, 5% -

10

% of women with

GDM

continue to have high

BG levels

and are diagnosed as having diabetes, usually

T2DM. 35-60% of women with GDM develop T2DM in 10-20 years.

At risk for recurrent GDM

with future

pregnancies.

Treatment: diet, exercise, insulin

BG goals:

< 95mg/

dL

pre-prandial

< 130-140mg/

dL

1 hour post-prandial

< 120mg/

dL

2 hours post-prandial

Slide75

Monogenic Diabetes

Two forms: Maturity Onset Diabetes of the Young (MODY) and Neonatal Diabetes Mellitus

1-5% of U.S. diabetics have monogenic diabetes, usually MODY

Due to mutations in a single gene

20 genes have been implicated in the development of monogenic diabetes

May happen spontaneously BUT has strong hereditary component

Management depends on severity of disease

Genetic testing of family members necessary

Slide76

Maturity Onset Diabetes of the Young (MODY)

More common than Neonatal Diabetes

Often

misdiagnosed as T1DM if found in adolescence or T2DM if later in life

Presentation

depends on severity; hyperglycemia may be discovered on routine lab

work

Each

child has a 50% chance of inheriting the MODY gene

Most

commonly caused by mutations in the 

HNF1A

 gene or the 

GCK 

gene

Slide77

Neonatal Diabetes Mellitus

First 6 months of life Symptoms similar to that of T1DM Most commonly caused by mutations in the KCNJ11, ABCC8 or INS genesManagement same as T1DM (need to replace insulin)

Slide78

Medications: Oral Agents

Alone, only lower HbA1c 1-2% (

Faulds

, 2014)

Can combine agents with different mechanisms of action (

Faulds

, 2014)

With combination, can only decrease HbA1c by 2-3% (

Faulds

, 2014)

Insulin

Secretagogues

: action increases secretion of insulin by the beta cells

Sulfonylureas

Nonsulfonylurea

insulin

secretagogues

(

meglitinides

and phenylalanine derivatives)

Biguanides

Alpha-

glucosidase

inhibitors

Thiazolidinediones

(

glitazones

)

SEE TABLE 30-6 (pages 836-7) IN BOOK

Slide79

Sulfonylureas

Action: directly stimulate the pancreas to secrete insulin, increase insulin effectiveness at cellular level, decrease glucose production by the liver

Lower HbA1c by 1-2% (

Faulds

, 2014)

Must have a functioning pancreas, liver, kidneys

Side effects:

hypoglycemia;

mild GI; sulfa allergy; weight gain; interact with NSAIDs, warfarin, sulfonamides

Recommend not to take with beta blocker (mask symptoms of hypoglycemia)

No alcohol

Second-generation fewer side effects, drug interactions, excreted by liver and kidneys

Glipizide, glyburide, glimepiride

Slide80

Non sulfonylurea Insulin Secretagogues

Action: similar action as sulfonylureasDecrease HbA1c by 1-2% (Faulds, 2014)Rapid onset, short duration  must be taken with mealsSide effects: hypoglycemia; weight gain (less than Sulf.); interactions with ketoconazole, fluconazole, erythromycin, rifampin, isoniazidrepaglinide (Prandin), naglitinide (Starlix)

Slide81

Biguanides

Action:

decreasing hepatic production of glucose, facilitate action of insulin on peripheral receptor sites

Lower HbA1c 1-2% (

Faulds

, 2014)

May be used with

Sulf

. to further lower BG

Do not use if renal or liver impairment, respiratory insufficiency, infection, alcohol abuse

Side effects: lactic acidosis, GI disruptions, drug interactions

D/c use 2 days prior to contrast administration (renal)

Metformin, metformin with glyburide

Slide82

Alpha-Glucosidase Inhibitors

Action: delay absorption of complex carbohydrates in intestine, slow entry of glucose into systemic circulation = lower post-prandial BG

Decrease HbA1c 0.5-1% (

Faulds

, 2014)

Side effects: hypoglycemia, GI side effects, drug interactions

Take with first bite of food

Monitor liver function

Do not use if renal or GI dysfunction, cirrhosis

a

carbose

(

Precose

),

miglitol

(

Glyset

)

Slide83

Thiazolidinediones

Action: Sensitize body tissue to insulin, stimulate insulin receptor sites

Decrease HbA1c 0.5-1% (

Faulds

, 2014)

May be used in combination with other meds

Side effects: hypoglycemia, anemia, weight gain, edema, liver dysfunction, drug interactions, hyperlipidemia, impaired platelet function, decrease effectiveness of oral contraceptives

p

ioglitazone (Actos), rosiglitazone (Avandia)

Slide84

DPP-4 Inhibitors/Incretin Enhancers

Action: stimulates release of insulin, prevents secretion of glucagon, slows postprandial gastric emptying

Decrease HbA1c 0.5-1% (

Faulds

, 2014)

Side effects: may promote weight loss, GI disturbances, hypoglycemia, pancreatitis

Combination with metformin or

Sulf

.

s

itagliptin

(Januvia),

saxaglipton

(

Onglyza

),

exenatide

(

Byetta

)

Slide85

Slide86

Who gets insulin? (Dungan, 2014)

All T1DM

Depending on severity, GDM (pregnancy)

Eventually, most T2DM

At the time of diagnosis, approximately 50% of beta cell function is lost

Only a matter of time (average about 10 years) before require insulin

HbA1c > 8% on two oral agents

Unable to take oral agents

HbA1c > 10%

Symptomatic

Other

Hospitalization

Corticosteroid administration

Infection

Cost

Slide87

Slide88

Medications: Insulin

Onset, peak, duration, concentration, route

See page 830, Table 30-4 for insulin regimens

“Think like a pancreas!”

Fast-acting (includes rapid- and short-acting), intermediate-acting, long-acting

Basal and bolus coverage

Common basal insulin (long-acting)

Detemir

,

Glargine

, NPH

Common bolus insulin (fast- and intermediate-acting; sliding

scale insulin for BG and carbohydrate

coverage)

Regular,

lispro

,

aspart

,

glulisine

Slide89

Insulin Activity

Slide90

Slide91

Slide92

Basal Insulin

Provides coverage throughout the day

Syringe, pen, pump

Intermediate acting – cloudy

NPH (

Humulin

N,

Novolin

N)

Long acting – DO NOT MIX

Glargine

(Lantus)

Detemir

(

Levemir

)

Slide93

Bolus Insulin

Rapid-acting

Lispro

(Humalog)

Aspart

(

Novolog

)

Glulisine

(

Apidra

)

Short-acting

Regular (

Humulin

R,

Novolin

R)

Slide94

Pros:Better mealtime flexibility and coverageLess hypoglycemiaBasal coverage throughout the dayBetter reproducibility of glycemic effects

Cons:Multiple injections per dayCannot mix insulinsMore expensive

B

L

S

Hs

B

Meals

Insulin Effect

Multi- dose insulin using insulin analogs

Aspart: 50% of total daily dose divided over 3 meals (Ex. 5 unit SQ QAC)

Glargine: 50% of total daily dose (Ex. 15 units QHS)

Slide95

Combination Insulin

Novolin

70/30 (

Humulin

70/30)

70% NPH

30% Regular

Humulin

50/50

50% each NPH and Regular

Novolog

Mix 70/30

70%

Aspart

protamine suspension

30%

Aspart

Humalog Mix 75/25

75%

Lispro

protamine suspension

25%

Lispro

Humalog Mix 50/50

50% each

Lispro

protamine suspension and

Lispro

Slide96

Twice-daily Split-mixed Regimens

Regular

NPH

B

S

L

HS

Insulin Effect

B

70/30 insulin: 70% NPH, 30% Regular

2/3 should be given before breakfast, 1/3 before supper

Slide97

Medication calculation

Carbohydrate count5 grams of CHO to 1 unit of insulin for tightest controlCan also be 10, 15, or 20 grams CHO: 1 unit Sliding scale insulin (SSI) for BGOften 1 unit for every 50 mg/dL over 150 mg/dLDifferent for every person

Slide98

Calculation Practice

Pre-lunch BG: 204 mg/

dL

SSI order states to give 1 unit of

aspart

insulin for every 50 mg/

dL

over 150 mg/

dL

How much to give?

Planning to eat turkey sandwich with mustard (45 grams), unsweetened iced tea (0 grams), small apple (25 grams), and 1 cup carrots (12 grams) with ranch dressing (2 grams) = 84 grams total

Order states 10 grams CHO: 1 unit

aspart

insulin

How much to give?

Slide99

Insulin Administration

Store in refrigerator EXCEPT the current vial, which is stored at room temperature (good for 1 month) Inspect for clarity, precipitate, flocculation (frosted, whitish coating inside bottle)Check expiration date, opening dateRoll vial between hands (do not shake)Pen versus syringe/needleSyringe selection 1ml, .5ml, .3ml27 or 29 gauge needle, 0.5 inches longMay draw up insulin up to 3 weeks early, store with needle in upright positionSubcutaneous sites: posterior arms, anterior thighs, hips, abdomenRotate sites to prevent lipodystrophySee page 832-3 for instructions

Slide100

Insulin Administration

Slide101

Insulin Administration Complications

Insulin

resistance

Morning hyperglycemia

Dawn phenomenon: relatively normal BG until 3am, due to nocturnal surges in growth hormone secretions

Somogyi

effect: nocturnal hypoglycemia with rebound hyperglycemia

Insulin waning: progressive increase in BG from bedtime to morning

Local allergic reaction 1-2 hours after administration

Systemic allergic reaction (hives) – rare

Lipodystrophy

Lipoatrophy

: loss of subcutaneous fat, slight dimpling or pitting of subcutaneous fat

Lipohypertrophy

:

fibrofatty

mass, raised and hardened tissue

Slide102

Other Forms of Insulin

Continuous Subcutaneous Insulin Infusion (CSII) pump U-500 insulinMost insulin is 100 units/1 mL, this is 5 TIMES the normal concentrationHigh-risk medicationUsed for those with poor absorption, insulin resistance, large doses

Slide103

Other Forms of Insulin, cont.

Inhaled insulin Fast absorptionNot for those with lung disease Pre-mealExubera 2006-2007Afrezza http://www.webmd.com/diabetes/news/20140630/inhaled-insulin-afrezza Peak 15-20 minutes, duration 2-3 hours Less weight gainFewer episodes, less severe hypoglycemia

Slide104

Patient Teaching

Gerontologic

Considerations

– page2 821-22 (Box 30-4)

Medications

Physical activity

Nutrition

Self-monitoring of blood glucose (SMBG)

Care for the following:

Feet

Eyes

Kidneys

Heart/brain

Mental health

Teeth

Also higher risk for fatty liver disease

Slide105

Gerontologic Considerations

Age-related changes make diabetes management difficultSee Box 30-4 on page 822

Slide106

Teaching: Medications

Slide107

Teaching: Physical Activity

Goal

>

150 minutes per week

Weight control, improve insulin utilization, ease stress, CVD risk factor improvement (i.e., lower lipids, increase HDL, decrease total cholesterol and triglycerides)

Slow, gradual increase

Consistent, daily exercise

For those who take insulin, may need a snack after exercise to avoid hypoglycemia

Slide108

Teaching: SMBG

T2DM who are not on insulin



2-3 times per week, including a 2-hour post-prandial, also during medication changes or suspected hyper- or hypoglycemia

If on insulin

 before meals and at bedtime,

suspected hyper- or hypoglycemia

Continuous Glucose Monitoring (CGM)

Urine Glucose Testing: renal threshold for glucose is 180-200 mg/

dL

(affected by age and renal function)

Keep a logbook/record

There’s an (well, more than one!) app for that.

Slide109

Teaching: Nutrition

Consistent carbohydrate and caloric intake, at consistent intervals (especially for those who take insulin) – to prevent hypoglycemia

Personalize care: consider lifestyle, preferences, culture, ethnicity, eating times

Include skills such as reading labels, eating out, adjusting meal plan for special occasions/illness/exercise

Exchange List for Meal Planning – see page 824-5

and

http://

www.nhlbi.nih.gov/health/educational/lose_wt/eat/fd_exch.htm

Create

Your Plate:

http://www.diabetes.org/food-and-fitness/food/planning-meals/create-your-plate

/

50-60% calories from carbohydrates, 20-30% from fat (cholesterol less than 200mg/day, saturated fat <7%), 10-20% from protein

Fiber

Soluble: legumes, oats, fruits (help lower LDL and BG)

Insoluble: whole grains, cereals, vegetables

Slide110

Create Your Plate

Slide111

Inpatient Diabetes Management

Usually hyperglycemia, but also hypoglycemia

Typically discontinue oral agents, switch to bolus insulin (

lispro

and

aspart

are commonly used at OSUWMC) –

why no oral agents?

Acute illnesses = hyperglycemia

Steroid administration

NPO for procedure, etc.

Electrolyte management

Slide112

Treatment

Patient Predisposition

Illness

Hyperglycemia

Pancreatic reserve

Insulin resistance

Catecholamines

HPA axis activationInflammatory cytokinesLipotoxicity

Exogenous glucocorticoids

VasopressorsTotal parenteral nutritionEnteral nutrition

Etiology of Hospital Related Hyperglycemia

Slide113

Complications requiring hospitalization: Diabetic Ketoacidosis (DKA)

Caused by lack of insulin

Results in hyperglycemia, ketosis, dehydration, electrolyte loss, acidosis

No insulin = glucose does not enter cells but stays in plasma; liver releases glucose; kidneys attempt to get rid of extra glucose by osmotic diuresis = dehydration and electrolyte loss

Breakdown of fat into free fatty acids and glycerol (see previous slides)

 converted into ketone bodies by liver 

metabolic acidosis

ABG: pH low, bicarbonate low, CO

2

normal

Attempt to correct low pH and low bicarbonate by “blowing off” CO

2

=

Kussmal

respirations

Slide114

DKA Signs/Symptoms

Polyuria

Polydypsia

Diagnostic

pH 6.8-7.3

BG > 250 mg/

dL

Serum bicarbonate low (0-15mEq/L0

Serum and urine ketones

Glucose in urine

Na, K, Cl serum levels abnormal – how?!?

Anion gap

Blurred vision (osmotic changes on the lens)

SEE FIGURE 30-7 on page 842

Osmotic diuresis



Water and electrolyte loss

 dehydration  circulatory failure

Metabolic acidosis

 CNS depression  coma

Slide115

DKA Management

Correct dehydration, electrolyte loss, acidosis

6-10 L of IV fluids! (But not too quickly, due to risk for cerebral edema.) Start with NS, then to dextrose-containing fluids when BG < 250 mg/

dL

.

Frequent VS monitoring – respiratory, cardiac, neurological, intake/output balance . Ensure your patient is not fluid overloaded!

K and Cl replacement – most important to monitor K levels q2-4h

WHY DOES K SHIFT IN/OUT OF CELLS?!

Acidosis reversed by insulin administration

Insulin

gtt

Do not lower BG too quickly!

Hourly BG checks

Dextrose when BG < 250mg/

dL

See

OSUWMC policy:

https://

onesource.osumc.edu/sites/ebm/Documents/Guidelines/Type1Diabetes.pdf

Slide116

Complications requiring hospitalization: Hyperglycemic Hyperosmolar (non-ketotic acidosis) Syndrome

How is it different than DKA?

 NO KETOSIS OR ACIDOSIS (insulin is still present)

Mortality rate 10-40%

Hyperosmolality

(

>

340mOsm/L) and hyperglycemia (> 600mg/

dL

) with minimal or no ketosis

Older, 50-70

y.o

., with or without T2DM

Precipitating events: infection, acute or chronic illness, procedures such as dialysis or surgery, medications

Slide117

HHNS Signs/Symptoms

Hypotension

Dehydration (more than DKA)

Tachycardia

Neurologic signs due to cerebral dehydration from

hyperosmolality

Sensory alterations

Seizures

Hemiparesis

Slide118

HHNS Management

Same as DKA, minus anion gap monitoring

Be

very

careful of fluid status (older patients)!

See

OSUWMC policy:

https://

onesource.osumc.edu/sites/ebm/Documents/Guidelines/Type2Diabetes.pdf

Slide119

Complication requiring hospitalization: Hypoglycemia

Causes: too much insulin or OHA, too little food, excessive PAOften prior to mealsThink about insulin profiles – when does it peak?

Slide120

Hypoglycemia: Symptoms

DIFFERENT FOR EVERY PERSON

Autonomic Nervous System (ANS) (onset)

Epinephrine, Norepinephrine released

Sweating, tremor, tachycardia, palpitations, anxiety, hunger

Central Nervous System (CNS) (intermediate)

Brain cells do not have fuel

Impaired concentration, headache, lightheaded, dizzy, confusion, forgetful, numb lips/tongue, slurred speech, impaired coordination, labile emotions, irrational or combative behavior, double vision, drowsiness

CNS (severe)

Disoriented, seizures, somnolence, LOC

Slide121

Hypoglycemia: Management

IF ABLE TO SWALLOW SAFELY, Give CHO

15 grams of fast-acting carbohydrate PO

3-4 glucose tablets

4-6

oz

fruit juice or soda (non-diet)

6-10 hard candies

2-3 TBL sugar/honey

Retest BG within 15 minutes; retreat if less than 0-75 mg/

dL

Plus snack with protein and starch within 30-60 minutes (once symptoms resolve)

Slide122

Hypoglycemia: Management

Glucagon 1 mg SQ or IM

25-50 mL (12.5-25 g) of 50% D

50

W via IVP at 10mL/min

Be sure to evaluate if patient has insight to hypoglycemia, re-evaluate BG 15 minutes after intervention

See OSUWMC policy for

hypoglycemia management:

https://

onesource.osumc.edu/sites/diabetes/Documents/Hypoglycemia.pdf

Slide123

Have a great day!

http://whatshouldwecallnursing.tumblr.com

/

http://whatshouldwecallnursingschool.tumblr.com

/

Have a wonderful semester!!!!!



Slide124

References

American Association of Diabetes Educators (AADE). (2014). Diabetes Tip Sheets. Retrieved May 27, 2014, from

http://www.diabeteseducator.org/DiabetesEducation/PWD_Web_Pages/Holiday_Eating_Patient_Resources.html

.

American Diabetes Association (ADA). (2013, March 6). American Diabetes Association Releases New Research Estimating Annual Cost of Diabetes at $245 billion. Retrieved December 1, 2013, from

http://www.diabetes.org/for-media/2013/annual-costs-of-diabetes-2013.html?loc=cost-of-diabetes

.

American Diabetes Association (ADA). (2010). Diagnosis and classification of diabetes mellitus.

Diabetes Care, 33

(S1).

American Diabetes Association (ADA). (2012). Standards of medical care in diabetes. 

Diabetes Care, 35

(S1), S12, table 2. Retrieved October 14, 2014 from http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/.

American Heart Association (AHA). (2014). About metabolic syndrome.

American Heart Association.

Retrieved October 14, 2014, from http://www.heart.org/HEARTORG/Conditions/More/MetabolicSyndrome/About-Metabolic-Syndrome_UCM_301920_Article.jsp.

Aljasem

, L.I.,

Peyrot

, M.,

Wissow

, L., & Rubin, R.R. (2001). The impact of barriers and self-efficacy on self-care behaviors in type 2 diabetes.

Diabetes Educator, 27

(3).

Atak

, N.,

Gurkan

, T., &

Kose

, K. (2008). The effect of education on knowledge, self-management behaviors, and self-efficacy of patients with type 2 diabetes.

Australian Journal of Advanced Nursing, 26

(2), 66.

Atkinson, M.A. (2012). The pathogenesis and natural history of type 1 diabetes.

Cold Spring Harbor Perspectives in Medicine.

Centers for Disease Control and Prevention (CDC). (2014).

National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014.

Atlanta, GA: U.S. Department of Health and Human Services.

Center for Disease Control and Prevention (CDC). (2014).

Prediabetes

.

Diabetes Public Health Resource

. Retrieved October 14, 2014, from http://www.cdc.gov/diabetes/consumer/prediabetes.htm.

Chen, C-P., Peng, Y-S.,

Weng

, H-H., Yen, H-Y., & Chen, M-Y. (2013). Health-promoting behavior is positively associated with diabetic control among type 2 diabetes patients.

Open Journal of Nursing, 3,

274.

Diabetes Control and Complications Trial Research Group (DCCT). (1993). The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin-dependent diabetes mellitus.

New England Journal of Medicine, 329

, 977–986.

Dungan, K. (2014).

Insulin in Inpatients and Outpatients

[

Powerpoint

slides]. Presentation, May 2014.

JDRF. (

n.d.

). Type 1 Diabetes Facts. Retrieved October 15, 2014, from http://jdrf.org/about-jdrf/fact-sheets/type-1-diabetes-facts/.

Faulds

, E.R. (2014). Pharmacological Management of Type 2 Diabetes: Oral Medications and Noninsulin

Injectables

[

Powerpoint

slides]. Nursing 6111, May 2014.

 

 

 

 

 

 

Slide125

References

King, D.K., Glasgow, R.E.,

Toobert

, D.J.,

Strycker

, L.A.,

Estabrooks

, P.A.,

Osuna

, D., & Faber, A.J. (2010). Self-efficacy, problem solving, and social-environmental support are associated with diabetes self-management behaviors.

Diabetes Care, 33

, 751-753.

King, P., Peacock, P., & Donnelly, R. (1999). The UK Prospective Diabetes Study (UKPDS): Clinical and therapeutic implications for type 2 diabetes.

British Journal of Clinical Pharmacology, 48

(5), 643-648.

Lightsey

, R. (2011). Diagnosis and treatment of latent autoimmune diabetes in adults still evolving.

ClinicalAdvisor

.

Retrieved October 13, 2014, from http://www.clinicaladvisor.com/diagnosis-and-treatment-of-latent-autoimmune-diabetes-in-adults-still-evolving/article/203578/.

Longhurst

, A.S. (2014).

Type 2 Diabetes Statistics and Facts

. Retrieved October 15, 2014, from http://www.healthline.com/health/type-2-diabetes/statistics#1.

Mercola

, J. (2014). Sugar Consumption Accounts for a Big Chunk of Health Care Costs. Retrieved May 27, 2014, from

http://articles.mercola.com/sites/articles/archive/2014/03/29/sugar-consumption-healthcare-costs.aspx

.

National

Institute of Diabetes, Digestive and Kidney Diseases (NIDDK). (2007).

Monogenic forms of diabetes: Neonatal diabetes mellitus and maturity-onset diabetes of the young

(NIH Publication No. 07-6141). Bethesda, MD: National Diabetes Information Clearinghouse.

National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK). (2011). National Diabetes Statistics, 2011. Retrieved from May 27, 2014, from

http://diabetes.niddk.nih.gov/dm/pubs/statistics/#fast

.

Nordlie

, R.C., Foster, J.D., & Lange, A.J. (1999). Regulation of glucose production by the liver.

Annual Review of Nutrition, 19,

379-406.

Osborn, C.Y.,

Bains

, S.S., &

Egede

, LE. (2010). Health literacy, diabetes self-care, and glycemic control in adults with type 2 diabetes.

Diabetes Technology & Therapeutics, 12

(11), 913.

Pellico

, L.H. (2013).

Focus on Adult Health Medical Surgical Nursing.

Lippincott Williams & Wilkins: Philadelphia, PA.

Pessin

, J.E., &

Saltiel

, A.R. (2000). Signaling pathways in insulin action: Molecular targets of insulin resistance.

The Journal of Clinical Investigation, 106

(2), 165-169.

Saltiel

, A.R. (2000). Series Introduction: The molecular and physiological basis of insulin resistance: Emerging implications for metabolic and cardiovascular diseases.

Journal of Clinical Investigation, 106

(2), 163-164. doi:10.1172/JCI10533.

Stratton, I.M., Adler, A.I., Andrew, H., Neil, W., Matthews, D.R., Manley, S.E., Cull, C.A.,

Hadden

, D. , Turner, R.C., Holman, R.R. (on behalf of the U.K. Prospective Diabetes Study Group). (2000). Association of

glycemia

with

macrovascular

and microvascular complications of type 2 diabetes (UKPDS 35): Prospective observational study.

British Medical Journal, 321

, 405–412.

University of California San Francisco (UCSF). (2014). The liver and blood sugar.

Diabetes Education Online.

Retrieved October 14, 2014 from http://dtc.ucsf.edu/types-of-diabetes/type2/understanding-type-2-diabetes/how-the-body-processes-sugar/the-liver-blood-sugar/.

United States Department of Agriculture (USDA). (

n.d.

). ChooseMyPlate.gov. Retrieved from May 27, 2014, from

http://www.choosemyplate.gov/

.