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Chronic Illness: Diabetes and Devastating Depression. Total Healthcare of Michigan, P.C. 2900 Hannah Boulevard, Suite 200 East Lansing, MI 48823 Phone: (517) 332-0440. Chronic Illness: Diabetes and Devastating Depression. Chronic Illness: Diabetes and Devastating Depression.

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Total healthcare of michigan p c l.jpg

Chronic Illness: Diabetes and Devastating Depression

Total Healthcare of Michigan, P.C.

2900 Hannah Boulevard, Suite 200East Lansing, MI 48823

Phone: (517) 332-0440



Chronic illness diabetes and devastating depression3 l.jpg
Chronic Illness: Diabetes and Devastating Depression

Anderson at al, Diabetes Care 24: 1069 – 1078, 2001

  • 39 Studies

  • N = 20,218


Chronic illness diabetes and devastating depression results l.jpg
Chronic Illness: Diabetes and Devastating DepressionResults

Diabetes….

  • Diabetics have 2 times the risk for depression than non-diabetics

  • Women > Men prevalence

  • 1:3 women had depression

    Impaired….

  • Level of functioning

  • Quality of life

  • Adherence to medical treatment, therefore, impaired glycemic control

    Increased…

  • Risk of diabetes complications


Chronic illness diabetes and devastating depression prospective studies l.jpg
Chronic Illness: Diabetes and Devastating DepressionProspective Studies

Depression a risk factor for Type II Diabetes

  • Treatment of Major Depression Disorder, increased glycemic control

  • However, only 1 in 3 cases are treated for depression

  • An increase in HGB1AC (with psych hx) – Cohen et al 1977

  • Treatment of Depression decreased HGB1AC – Hustman et al 1997

    Source: General Hospital Psychiatry: 1997; Psycho Med:1997


Chronic illness diabetes and devastating depression hmo statistics l.jpg
Chronic Illness: Diabetes and Devastating DepressionHMO Statistics

  • Chronic Medical/MDD 24.7%

  • No Medical/MDD 17.5%

  • Diabetes/MDD 22.7%

    (Wells et al AMJP; 1988)

  • Diabetes with MDD showed increased…

    Visits to PCP

    Visits to ER

    (Diabetes Care; 2003; 26: 104-111)


Leading causes of disease burden for women in the us in 1996 l.jpg
Leading Causes of Disease Burden for Women in the US in 1996

*Also includes other degenerative and hereditary CNS disorders

Michaud CM., et al. JAMA. 2001;285:535-539


Common presenting somatic complaints in patients with depression l.jpg

Tired all the time, “blahs”

Sexual dysfunction or loss of sexual interest

Vague abdominal or joint pains

Disturbed sleep

Headache

“Stressed out”

Malaise

GI complaints (i.e., constipation, diarrhea)

Common Presenting Somatic Complaints in Patients with Depression

DSM-IV-TR Washington DC: American Psychiatric Association: 2000.

Mulsant, BH, Ganguli M. J Clin Psychiatry. 1999: 60(suppl 20):9-15.


Common presenting psychological symptoms in patients with depression l.jpg

Hopelessness

Low self-esteem

Impaired memory

Difficulty

Anhedonia

Anxiety

Preoccupation with negative thoughts

Common Presenting Psychological Symptoms in Patients with Depression

DSM-IV-TR Washington DC: American Psychiatric Association: 2000.

Mulsant, BH, Ganguli M. J Clin Psychiatry. 1999: 60(suppl 20):9-15.


Chronic nonmalignant pain cnp l.jpg
Chronic Nonmalignant Pain (CNP)

  • Myofacial Pain

    Low Back Pain

    Muscle Contraction (tension) Headaches

    Fibromyalgia

  • Nerve Injury Pain

    Neuropathic Pain

    Complex Regional Pain Syndrome (SMP)

  • Headaches

  • Arthritis


The cost of chronic nonmalignant pain to the u s economy l.jpg
The Cost of Chronic Nonmalignant Pain to the U.S. Economy

$ 90-100 Billion per Year

Direct costs of care

Lost productivity

Absenteeism

$ Quality of Life for Pain Suffers

Inability to work and recreate

Loss Function

Decrease perception of self worth


Economics of depression dimensions l.jpg
Economics of Depression: Dimensions

Quality of Life

Workplace Impact

Burden of Illness

DEPRESSION

Comparative Data

Cost of Drug Therapy

Cost of Therapy Failure


Impact of untreated depression l.jpg

Morbidity

Comorbid medical illness

Suicide attempts

Accidents

Mortality

35,000 suicides per year

Fatal accidents

Death due to related illness (substance abuse)

Societal and Functional Burdens

Dysfunctional families

Divorce

Substance abuse

Absenteeism

Decreased productivity

Job-related injuries

Lost jobs

Failure to advance in career or school

Impact of Untreated Depression

Preskorn, 1999


Depression may worsen outcomes of many general medical conditions l.jpg
Depression May Worsen Outcomes of Many General Medical Conditions

Depression also may worsen outcomes of cancer, diabetes, AIDS, and other disorders7

1. Frasure-Smith N, et al. JAMA. 1993;270:1819-1825.

2. Penninx BW, et al. Arch Gen Psychiatry. 2001;58:221-227.

3. Jiang W, et al. Arch Intern Med. 2001;161:1849-1856.

4. Vaccarino V, et al. J Am Coll Cardiol. 2001;38:199-205.

5. Rovner BW, et al. JAMA. 1991;265:993-996.

6. Pohjasvaara T, et al. Eur J Neurol. 2001;8:315-319.

7. Petitto JM, Evans DL. Depress Anxiety. 1998;8(suppl 1):80-84.


Psychoanalysis and pain l.jpg
Psychoanalysis and Pain Conditions

  • Pain referred to as somatization

  • Pain is a symbol of emotional conflict

  • Pain subsides as patient works through psychological conflicts in psychotherapy


Jacho 2001 revised standards for pain management l.jpg
JACHO 2001 ConditionsRevised Standards for Pain Management

  • Patients’ rights

  • Assessment of pain

  • Care of patients

  • Education of patient and family

  • Continuum of care

  • Improved organizational performance

http://www.jcaho.org.


Two thalamic pain outflows l.jpg
Two Thalamic Pain Outflows Conditions

Sensory Cortex

  • Location of pain

  • Affective context

  • Limbic System

  • Hedonic aspect of pain

  • Poorly localized

  • Causes agony & suffering


Emotions and pain l.jpg
Emotions and Pain Conditions

Negative Emotions Increase Pain

  • Sadness

  • Anger

  • Fear

Positive Emotions Decrease Pain

  • Joy

  • Humor

  • Sexual arousal

Unrelieved chronic pain often leads to depression and anxiety


Neuropathic pain l.jpg
Neuropathic Pain Conditions

  • Pain that originates in or is amplified by the CNS or direct injury to peripheral nerves

  • Often has an emotional component

  • Has a peculiar burning and aching quality

  • Less responsive to opioids


Referred pain spinal level l.jpg
Referred Pain: Spinal Level Conditions

  • Somatic & visceral afferents converge on a single dorsal horn neuron (e.g., left arm, heart)

  • Neurons sensitized by repetitive pain inputs from one source may respond as if all their inputs were activated

  • Severe pain input from heart can cause left arm pain


Referred pain limbic level l.jpg
Referred Pain: Limbic Level Conditions

  • Limbic neurons sensitized by ascending nociceptive pain signals may produce a wider range of negative affective states

  • Sustained, intense negative affective states may sensitize limbic neurons and create sensations of physical pain in the absence of peripheral nociception


Central sensitization l.jpg
Central Sensitization Conditions

  • Repeated negative inputs

  • Kindling

  • Neuroplasticity

  • Remodeling

  • Axonal sprouting


Sensitization l.jpg
Sensitization Conditions

Hyperalgesia

Allodynia

10

Injury

8

Normal

Pain

Response

6

Pain Intensity

Hyperalgesia – heightened sense of pain to noxious stimuli

Allodynia – pain resulting from normally painless stimuli

4

2

0

Stimulus Intensity

23

Gottschalk, Smith. Am Fam Physician. 2001;63:1979-1984.


Slide24 l.jpg

Risk Factors for Depression Conditions

Loss of a

parent before

age 10 y

Loss support

system of

social

Erectile

dysfunction†

Infertility

Low levels of

testosterone †

Risk Factors

Social or

economic

change †

Childhood hx

physical or

sexual abuse*

Personal hx of

mood disorders

in early reproductive

years *

Family hx

mood disorders

Persistent

psychosocial

stressors

* Risk factors that are greater for or specific to women.

† Risk factors that are greater for or specific to men.

Pajer K. J Clin Psychiatry. 1995;56(suppl2):30-37 Seidman SN, Walsh BT. Am J Geriatr Psychiatry. 1999;7:18-33

ACOG. Int J Gynecol Obstet. 1993;43:203-211 Morgan H. Aust Fam Physician. 2001;30:206-211


Theoretical contributions of nature and nurture to pathology l.jpg
Theoretical Contributions of ConditionsNature and Nurture to Pathology

Developmental

trajectory

Genetic factors

Enriched environment

Vulnerability and

resistance genes

Phenotypic

plasticity

Social support

Psychiatric

intervention

Trauma

Anxiety disorder

PTSD-like syndrome

Substance Abuse

HPA axis dysfunction

Psycho-immune

disease

Depression-like

syndrome

Vulnerability

Long-term

(mal)-adaptation

Adapted from: Plotsky PM, et al. Psychitr Clin North Am. 1998;21:293-307.


Gender specific differences in depression l.jpg
Gender-Specific Differences Conditionsin Depression

Parameters

Differences in Women vs Men

  • Seasonal effect on mood Greater1

  • Association with stressful More frequent2

    life events

  • Atypical symptoms of depression More common2(i.e., hypersomnia, hyperphagia)

  • Suicidal behavior

    • Suicide attempt More frequent3

    • Completed suicide Less frequent3

1. Leibenluft E, et al. Depression. 1995;3:13-19 2. Pajer K. J Clin Psychiatry. 1995;56(suppl2):30-37

3. Hirschfeld RM, Russel, JM. N Engl J Med. 1997;337:910-915


Mortality from nsaid induced gi complications versus other diseases in united states l.jpg
Mortality From NSAID – Induced GI Complications* ConditionsVersus Other Diseases in United States

25,000

20,000

15,000

10,000

5,000

0

20,197

16,685 16,500†

10,503

Number of Deaths

5,338

4,441

1,437

Leukemia1 HIV NSAIDs Multiple Asthma1 Cervical Hodgkin’s

GI2 Myleoma1 Cancer Disease

Cause of Death

  • Data from 1997†Estimated

  • National Center for Health Statistics, 1998;

  • Singh G, et al. J Rheumatol. 1999;26 (Suppl 56):18-24


Cox 2 and peripheral mechanisms of pain l.jpg
COX-2 and Peripheral Mechanisms of Pain Conditions

Tissue Injury

+

+

+

+

+

+

+

+

COX-2

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

P

+

+

+

EP

receptor

PKA

PKCe

PGE2

Resting

Membrane

Potential

Increases

SNS/PN3

TTX-resistant

sodium

channel

Neuron FiringThreshold Decreases

Samad et al. Nature. 2001;410:471-475; Woolf, Salter. Science. 2000;288:1765-1769;Byers, Bonica. In: Bonica’s Management of Pain. 2001:27-72.


Pathophysiology of cox 1 cox 2 and cox 3 l.jpg
Pathophysiology of ConditionsCOX-1, COX-2, and COX-3

Glucocorticoids

(block mRNA expression)

Acetaminophen

(–)

COXIBs

(–)

COX-1

Normal Constituent

COX-3

COX-2

(–)

(–)

Inducible

Normal Constituent

Normal Constituent

(–)

(–)

(–)

NSAIDs

  • HOUSEKEEPING

  • Stomach

  • Intestine

  • Kidney

  • Platelets

  • NORMAL CONSTITUENT

  • CNS Pain - Fever

  • Heart

  • Aorta

  • INFLAMMATORY SITE

    • Macrophages

    • Synoviocytes

    • Endothelial cells

  • NORMAL CONSTITUENT

  • CNS

  • Kidney

  • Female U/G tract

Arachidonic Acid


Arthritis pain management key recommendations common to the aps acr and ags guidelines l.jpg
Arthritis Pain Management: Key Recommendations Common to the APS, ACR, and AGS Guidelines

  • Start with acetaminophen because of cost, efficacy, and low toxicity

  • COX-2s for those at risk of GI complications or those who “require long-term, daily analgesic therapy” AGS 2002

  • Non-selective NSAIDs: GI risk assessment and use of cytoprotective agents

  • Opioids for severe pain or pain not controlled by APAP and/or COX-2s

APS=American Pain Society; ACR=American College of Rheumatology; AGS=American Geriatric Society.

Adapted from American Pain Society, 2002; ACR Subcommittee on OA Guidelines. Arthritis Rheum. 2000;43:1905-1915; Adapted from American Geriatric Society, 2002.


Malalignment l.jpg
Malalignment APS, ACR, and AGS Guidelines

From the Clinical Slide Collection on the Rheumatic Diseases, 1991, 1995, 1997

American College of Rheumatology


Platelet function trials celecoxib vs nsaids trials 032 and 065 l.jpg
Platelet Function Trials: Celecoxib vs NSAIDS (Trials 032 and 065)

Platelet Aggregation at Steady State

Placebo

Celecoxib 600 mg BID

Naproxen 500 mg BID

Ibuprofen 800 mg TID

Diclofenac 75 mg BID

100

80

60

40

20

0

Platelet Aggregation (%)

*

*

*

Trial 0321 (N = 24) Trial 0652 (N = 51)

Day 10 Day 8

*P<0.05 vs placebo; † P<o.5 vs celecoxib

1. Leese PT, et al. J Clin Pharmacol. 2000;40:124-132;2. Data on file, Searle, a division of Pharmacia Corporation


Pre and postoperative valdecoxib in patients undergoing hip arthroplasty opioid use l.jpg
Pre- and Postoperative Valdecoxib in Patients Undergoing Hip Arthroplasty: Opioid Use

50

40

30

20

10

0

Reduction in Morphine Consumption With Valdecoxib

Cumulative Amount of PCA and Bolus Morphine Used Postsurgery

41% with 40 mg dose43% with 20 mg dose

*

*

Mean Amount of Morphine Consumed (mg)

*

*

Placebo + MSO4 (n=71)

Valdecoxib 40 mg bid + MSO4 (n=73)

Valdecoxib 20 mg bid + MSO4 (n=73)

0

4

8

12

16

20

24

28

32

36

40

44

48

Hours

*P<0.001 valdecoxib 20 mg or 40 mg vs placebo.

Camu et al. Am J Ther. 2002;9:43-51.


Summary l.jpg
Summary Arthroplasty: Opioid Use


Summary safety of celecoxib l.jpg
Summary: Safety of Celecoxib Arthroplasty: Opioid Use

  • Upper Gastrointestinal Tract

  • Celecoxib was associated with a significantly lower incidence of endoscopic ulcers compared with naproxen 500 mg BID

  • A correlation between endoscopic ulceration and clinically serious upper GI events has not been fully established

  • Platelet Function

  • No significant effect on platelet aggregation and bleeding time

  • Liver Function Tests

  • Elevations in liver enzymes similar to placebo


Multidimensional treatment l.jpg
Multidimensional Treatment Arthroplasty: Opioid Use

  • No one specialty comprises the full range of knowledge and skills to evaluate and treat chronic pain

  • High frequency of limbic sensitization in chronic pain requires behavioral health evaluation & treatment


Coanalgesics l.jpg
Coanalgesics Arthroplasty: Opioid Use

Potentiate opioids & target neuropathic pain

  • Antidepressants / Anxiolytics

  • Anticonvulsants

  • Psychostimulants

  • Serotonin Dopamine Antagonists (SDAs)

  • Psychotherapy


Opioid monotherapy l.jpg
Opioid Monotherapy Arthroplasty: Opioid Use

  • Higher rate of incomplete pain relief

    (response but not remission)

  • May result in higher doses of opioids

  • Complications & shortfalls of opioid monotherapy, especially in chronic neuropathic pain states, may lead to invalid conclusions about the effectiveness and safety of opioids


Leading causes of disease burden for women in the us in 199639 l.jpg
Leading Causes of Disease Burden for Women in the US in 1996 Arthroplasty: Opioid Use

*Also includes other degenerative and hereditary CNS disorders

Michaud CM., et al. JAMA. 2001;285:535-539


Role of serotonin in the cns l.jpg
Role of Serotonin in the CNS Arthroplasty: Opioid Use

Serotonin modulates various brain functions

Mood

Cognition

Sensory perception

Temperature regulation

Nociception

(i.e., migraine headache)

Sexual behavior

Sleep

Appetite


Chronic illness diabetes and devastating depression41 l.jpg
Chronic Illness: Diabetes and Devastating Depression Arthroplasty: Opioid Use

Norepinephrine

Serotonin

Anxiety

Irritability

Energy

interest

Impulsivity

Mood, emotion,

cognitive function

Sex

Appetite

Aggression

Motivation

Drive

Dopamine


The evolution of antidepressants l.jpg
The Evolution of Antidepressants Arthroplasty: Opioid Use

1950s

1960s

1970s

1980s

1990s

Imipramine Clomipramine Maprotiline Fluoxetine Nefazodone

(1957) Nortriptyline Amoxapine Sertraline Mirtazapine

Amitriptyline Paroxetine Venalfaxine

Desipramine Fluvoxamine

____________ Citalopram

Phenelzine

Isocarboxazid

Tranylcypromine



Model for chronic activation of stress responses in mdd l.jpg
Model for Chronic Activation of Stress Responses in MDD Complex

Despair

Reproduction

Slow wave sleep

Eating Immune function

Behavioral responses

Electrophysiologic responses

Hippocampus

Kindling

Pyramidal cell firing rate

Locus ceruleus firing rate

Anterior pituitary

CRF

Metabolic responses

ACTH

Gluconeogenesis

Lipolysis

Proteolysis

Insulin resistance

Inflammation

Locus ceruleus

HPA AXIS HYPERACTIVITY

Blood pressure

Heart rate

Blood sugar

GI blood flow

Glucocorticoids

Epinephrine

Norepinephrine

Autonomic responses

STRESSOR

CRF=corticotropin-releasing factor; ACTH=adrenocorticotropin.

Adapted from: Arborelius L, et al. J Endocrinol. 1999;160:1-12.


Consequences of chronic stress activation l.jpg
Consequences of Chronic Stress Activation Complex

STRESS

Increased survival and growth

Atrophy/death of neurons

Glucocorticoids

BDNF

BDNF

Glucocorticoids

Normal survival and growth

5-HT and NE

Antidepressants

Duman RS, et al. Biol Psychiatry. 2000;48:732-739.


Stressful life events as a trigger for depression progressively declines l.jpg
Stressful Life Events as a “Trigger” for Depression Progressively Declines

10

8

6

4

2

0

Risk (%) of depression onset per month

Likelihood of recent life stress*

0 2 4 6 8 10

Number of previous depressive episodes

“Kindling” Phenomenon

  • With increasing

  • depressive episodes:

  • Risk of depression rises

  • Association with stressful life events declines

Risk

*Odds ratio for at least 1 stressful life event during month with a depressive episode.

Kendler KS, et al. Am J Psychiatry. 2000;157:1243-1251.


Hamd for 52 weeks l.jpg
HAMD For 52 Weeks Progressively Declines


Vas scale for pain 52 weeks l.jpg
VAS SCALE FOR PAIN:52 WEEKS Progressively Declines


Quality of life scale l.jpg
Quality of Life Scale Progressively Declines

  • START: 20.56

  • END/52 WEEKS: 80.77

  • MAXIMUM POINTS: 120


Healthplus of michigan pharmacologic step protocol for major depression l.jpg
HealthPlus of Michigan Progressively DeclinesPharmacologic Step Protocol for Major Depression

SSRI1

(Prozac*®, Paxil®, Zoloft®, Celexa®

*prozac is available as generic

DRAFT

Side effects noted Complaint of or persistent

(eg. GI intolerance) insomnia

Reduce dose if needed (SSRIs

are all equally effective with

comparable tolerability

  • Add low dose (50-100

  • trazodone QHS2

  • Consider Ambien ®/Sonata ® if

  • failed trazodone

1. Allow 8-12 weeks to see the full therapeutic effect (insomnia or somatic

complaint of pain can be part of symptomatic for depression)

2. If NOT responding within 4-6 weeks  SSRI gradually

3. If NOT responding after 8-12 weeks with MAXIMUM dose  considering

the following alternatives:

Draft Document

Page 1 of 3


Healthplus of michigan pharmacologic step protocol for major depression51 l.jpg
HealthPlus of Michigan Progressively DeclinesPharmacologic Step Protocol for Major Depression

Remeron®

1. Preferred in geriatric patients

with poor appetite or insomnia

2. Well-tolerated with no significant

drug interactions or dosage adjustment needed for renal dysfunction

Effexor® or Effexor XR®

1. Evidence has shown to be effective in moderate to severe type depression

2. May be associated with increased blood pressure (dose-dependent)

3. Effexor XR® provides slower rate of absorption and comparable drug exposure and plasma fluctuation as

immediate release

DRAFT

Allow 8-12 weeks for full therapeutic effect. For newly diagnosed episodes of depression, instruct your patient to continue to take the antidepressant for at least 6 months.

Page 2 of 3


Recurrence becomes more likely with each episode of depression l.jpg
Recurrence Becomes More Likely With Each Episode of Depression

First

episode

<50%

Second

episode

≈70%

Third +

episode

>90%

0 20 40 60 80 100

% of patients expected to experience recurrence

Stahl SM. Essential Psychopharmacology: Neuroscientific Basis and Practical Applications. 2nd ed. Cambridge, UK: Cambridge University Press; 2000:150.


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Chronic Pain and Diabetes Depression

Complementary Therapies

  • Occupational

  • Relaxation

  • Nutrition

  • Cognitive Restructuring


Total healthcare of michigan p c54 l.jpg

Chronic Illness: Diabetes and Devastating Depression Depression

Total Healthcare of Michigan, P.C.

2900 Hannah Boulevard, Suite 200East Lansing, MI 48823

Phone: (517) 332-0440


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