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Total Healthcare of Michigan, P.C.

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.

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

  2. Chronic Illness: Diabetes and Devastating Depression

  3. Chronic Illness: Diabetes and Devastating Depression Anderson at al, Diabetes Care 24: 1069 – 1078, 2001 • 39 Studies • N = 20,218

  4. 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

  5. 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

  6. 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)

  7. 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

  8. 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.

  9. 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.

  10. 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

  11. 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

  12. Economics of Depression: Dimensions Quality of Life Workplace Impact Burden of Illness DEPRESSION Comparative Data Cost of Drug Therapy Cost of Therapy Failure

  13. 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

  14. 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.

  15. Psychoanalysis and Pain • Pain referred to as somatization • Pain is a symbol of emotional conflict • Pain subsides as patient works through psychological conflicts in psychotherapy

  16. JACHO 2001Revised 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.

  17. Two Thalamic Pain Outflows Sensory Cortex • Location of pain • Affective context • Limbic System • Hedonic aspect of pain • Poorly localized • Causes agony & suffering

  18. Emotions and Pain Negative Emotions Increase Pain • Sadness • Anger • Fear Positive Emotions Decrease Pain • Joy • Humor • Sexual arousal Unrelieved chronic pain often leads to depression and anxiety

  19. Neuropathic Pain • 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

  20. Referred Pain: Spinal Level • 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

  21. Referred Pain: Limbic Level • 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

  22. Central Sensitization • Repeated negative inputs • Kindling • Neuroplasticity • Remodeling • Axonal sprouting

  23. Sensitization 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.

  24. Risk Factors for Depression 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

  25. Theoretical Contributions ofNature 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.

  26. Gender-Specific Differences in 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

  27. Mortality From NSAID – Induced GI Complications*Versus 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

  28. COX-2 and Peripheral Mechanisms of Pain 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.

  29. Pathophysiology of COX-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

  30. 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.

  31. Malalignment From the Clinical Slide Collection on the Rheumatic Diseases, 1991, 1995, 1997 American College of Rheumatology

  32. 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

  33. 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.

  34. Summary

  35. Summary: Safety of Celecoxib • 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

  36. Multidimensional Treatment • 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

  37. Coanalgesics Potentiate opioids & target neuropathic pain • Antidepressants / Anxiolytics • Anticonvulsants • Psychostimulants • Serotonin Dopamine Antagonists (SDAs) • Psychotherapy

  38. Opioid Monotherapy • 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

  39. 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

  40. Role of Serotonin in the CNS Serotonin modulates various brain functions Mood Cognition Sensory perception Temperature regulation Nociception (i.e., migraine headache) Sexual behavior Sleep Appetite

  41. Chronic Illness: Diabetes and Devastating Depression Norepinephrine Serotonin Anxiety Irritability Energy interest Impulsivity Mood, emotion, cognitive function Sex Appetite Aggression Motivation Drive Dopamine

  42. The Evolution of Antidepressants 1950s 1960s 1970s 1980s 1990s Imipramine Clomipramine Maprotiline Fluoxetine Nefazodone (1957) Nortriptyline Amoxapine Sertraline Mirtazapine Amitriptyline Paroxetine Venalfaxine Desipramine Fluvoxamine ____________ Citalopram Phenelzine Isocarboxazid Tranylcypromine

  43. Figure 1: A Schematic of the NMDAR-Associated Protein Complex

  44. Model for Chronic Activation of Stress Responses in MDD 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.

  45. Consequences of Chronic Stress Activation 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.

  46. 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.

  47. HAMD For 52 Weeks

  48. VAS SCALE FOR PAIN:52 WEEKS

  49. Quality of Life Scale • START: 20.56 • END/52 WEEKS: 80.77 • MAXIMUM POINTS: 120

  50. HealthPlus of MichiganPharmacologic 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

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