diabetes mellitus

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diabetes mellitus
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2010-11-05 22:11:04
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diabetes mellitus
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  1. The Facts
    • Diabetes is the 7th leading cause of death in the US
    • Affects 20.8 million Americans (7% of the population)
    • •6.2 million are undiagnosed and have developed complications without being aware of it
    • •High risk ethnic population
    • African Americans
    • Hispanic American
    • American Indian
    • Asian American
    • Asian Pacific Islander
  2. NEGATIVE FEEDBACK FOR LOW BLOOD GLUCOSE
    • LOW BLOOD GLUCOSE
    • PANCREAS
    • Glucagon released by Alpha cells of Pancreas
    • liver released glucose into blood
    • ACHIEVE NORMAL BLOOD GLUCOSE LEVEL
  3. NEGATIVE FEED BACK FOR HIGH BLOOD GLUCOSE
    • HIGH BLOOD GLUCOSE
    • PANCREAS
    • INSULIN RELEASED BY BETA CELLS OF PANCREAS
    • FAT CELLS TAKE IN GLUCOSE FROM BLOOD
    • ACHIEVE NORMAL BLOOD GLUCOSE LEVEL
  4. ROLE OF INSULIN
    • •Insulin:
    • Counters metabolic activity that would increase blood glucose levels
    • Enhances transport of glucose into body cells
    • Lowers blood glucose levels
  5. PHYSIOLOGY CONT
    INSULIN INJECTION TWO TYPE
    • BASAL (CONTINUOUS)
    • PRANDIAL (BOLUS)
  6. HORMONE THAT AFFECT BS
    HORMONE DECREASE BG
    • INSULIN
    • AMYLIN
    • GLP-1
  7. HORMONE THAT INCREASE EFFECT ON BG
    • GLUCAGON
    • EPINEPHRINE
    • GLUCOCERTICOIDS
    • GROWTH HORMONES
    • PROGESTERONE, HPL, CORTISOL
  8. DIABETES MELLITUS
    • •Diabetes Mellitus
    • •A disorder of carbohydrate, protein, and fat metabolism resulting from an imbalance between insulin Availability and insulin need. (Porth, 2002)
    • End Result : HYPERGLYCEMIA
  9. CLASSUFICATION OF DM
    GASTATIONAL DM
    • TYPE 1 IMMUNE MEDIATED
    • TYPE 2 INSULIN RESISTANCE
    • PRE-DIABETES
    • IMPAIRED FASTING GLUCOSE
    • IMPAIRED GLUCOSE TOLERANCE
  10. PHYSIOLOGY GLUCOSE CONTROL
    NORMAL PROCESS
    • 1 STOMACH CONVERTS FOOD TO GLUCOSE
    • 2 GLUCOSE ENTERS BLOODSTREAM
    • 3 PANCREAS PRODUCES INSULIN
    • 4 GLUCOSE ENTERS BODY EFFECTIVELY
    • 5 GLUCOSE LEVELS IN BALANCE
  11. PATHO DM TYPE I
    • 1,STOMACH CONVERTS FOOD TO GLUCOSE
    • 2. GLUCOSE ENTERS BLOOD STREAM
    • 3. PANCREAS PRODUCES LITTLE OR NO INSULIN
    • 4, GLUCOSE UNABLE TO ENTER BODY EFFECTIVELY
    • 5 GLUCOSE LEVEL INCREASE
  12. PATHO CONT; TYPE 2
    • 1. STOMACH CONVERTS FOOD TO GLUCOSE
    • 2. GLUCOSE ENTERS BLOODSTREAM
    • 3. PANCREAS PRODUCES SUFFICIENT INSULIN BUT IT IS RESISTANT TO EFFECTIVE USE
    • 4. GLUCOSE UNABLE TO ENTER BODY EFFECTIVELY
    • 5.GLUCOSE LEVELS INCREASE
  13. DM TYPE 1
    • No endogenous insulin
    • Tx requires insulin injections
    • Usually < age 30 yrs. But can occur later
    • Ketosis prone
    • (DKA)
    • Former names: IDDM (Juvenile)
    • Diabetes Type 1
    • Thin to normal body weight
    • Acute metabolic complications
    • (DKA)
  14. DM TYPE 2
    • Some endogenous insulin
    • Tx diet and exercise 1st, then pills and /or insulin
    • Usually over 30yrs. (peaks at 50), but can occur earlier
    • no ketosis
    • Former names:
    • NIDDM (maturity/adult- onset)
    • Diabetes Type 2
    • Usually Overweight
    • Chronic vascular complications
  15. DIABETES CLINICAL MANIFESTATIONS
    HYPERGLYCEMIA
    • POLYDYPSIA
    • POLYPHAGIA
    • POLYURIA
  16. •Diabetes Clinical Manifestations
    Cont: Signs and Symptoms
    Early signs
    • •3 Polys
    • •Weight loss
    • •Fatigue/Always tired
    • •VisualBlurring
  17. LATE SIGN
    • Late signs
    • •Any of the 3 Polys
    • •Frequent Infections
    • •Numbness/ tingling offeet or leg pain
    • •Slow healing wounds
    • •Chronic Complications
  18. SYMPTOMS OF HYPERGLYCEMIA
    • EXTREME THIRST
    • FREQUENT URINATION
    • DRY SKIN
    • BLURRED VISION
    • DROWSINESS
    • NAUSEA
    • HUNGER
  19. DIABETES: DX TESTS
    CHECK MD ORDER ACHS

    FASTING BLOOD GLUCOSE
    FBC < 100MG/DL
  20. ORAL GLUCOSE TOLERANCE TEST
    OGTT <140MG/DL
  21. GLYCOSYLATED HEMOGLOBIN
    HGBA1C 4-6
  22. DIABETES: DIAGNOSTIC TEST CONT
    GLYCOSYLATED HEMOGLOBIN TEST
    • MEASURE THE AMOUNT OF GLYCISYLATED HEMOGLOBIN(HEMOGLOBIN THAT IS CHEMICALLY LINKED TO GLUCOSE ) IN THE BLOOD
    • NORMAL 4-6 %
    • TARGET RANGE DM PT<7%
    • Hba1c check every 3 months
  23. CRITERIA FOR DIAGNOSIS OF DIABETES MELLITUS
    • Normal
    • –FPG <100 mg per dL
    • –2hr OGTT <140 mg per dL
    • Diabetes- positive findings from any two of the following tests on different days:
    • –Symptoms of diabetes mellitus* plus casual
    • (random) plasma glucose concentration >=200 mg / dL
    • or
    • –FPG >=126 mg per dL OR
    • 2hr OGTT >=200 mg per dL after a 75-g glucose load
  24. PRE DIABETES
    GLUCIDELINES FOR DX OF IFG AND IGT ARE
    • –Impaired Fasting Glucose (IFG)
    • FPG> 100 mg/dL but < 126 mg/dL

    • –Impaired Glucose Tolerance
    • •2 hr PC > 140 mg/dL but < 200 mg/dL
    • •Or 2 hr ogtt > 140 mg/dL but < 200 mg/dL
  25. DIABETES
    • DIABETES IS A GROUP OF METABOLIC DISEASE CHARACTERIZED BY
    • HYPERGLYCEMIA RESULTING FORM DEFECTS IN INSULIN SECRETION, INSULIN ACTION, OR BOTH
    • LONG TERM DAMAGE, DYSFUNCTION, AND ORGAN FAILURE ASSOCIATED WITH CHRONIC HYPERGLYCEMIA ESCPECIALLY
  26. DM FOR ORGAN
    EYE
    KIDNEY
    NERVES
    HEART AND BLOOD VESSELS
    • DIABETIC RETINOPATHY
    • DIABETIC NEPHROPATHY
    • DIABETIC NEUROPATHY
    • ATHEROSCLEROSIS, HTN, CARDIO AND CEREBROVASCULAR DISEASE
  27. LEADING CASES OF DM
    • NEW CASES OF BLINDNESS
    • END STAGE RENAL DISEASE
    • FOOT OR LEG AMPUTATION
  28. ACUTE COMPLICATION
    TYPE 1
    • DIABETIC KETOACIDOSIS(DKA)
    • BS>300 MG/DL
    • CLASSIC SYMPTOMS
    • KETOSIS
    • CHECK URINE FOR KETONES IF BS>300 MG/DL
  29. ACUTE COMPLICATION EMERFENCIES
    TYPE 2
    • HYPERGLYCEMIC HYPEROSMOLAR NON KETOTIC SYNDROME (HHNS)
    • BS>600MG/DL
    • SIMILAR SYMPTOMS
    • NO KETOSIS
  30. SICK DAY RULES
    • CHECK BG MORE FREQUENTLY( Q4H)
    • TEST URINE TO KETONES IF BS CONSISTENTLY HIGH >300MG/DL
    • CONTINUE WITH INSULIN AND ORAL HYPOGLYCEMICS
    • DRINK 8-12 GLASSES OF WATER
    • EAT MEALS AT REGULAR TIMES(SUBSTITUTE WITH HIGH CALORIE DRINKS IF EXPERIENCING ANOREXIA)
    • GET REST
  31. ACUTE COMPLICATIONS CONT
    HYPOGLYCEMIA TOO MUCH INSULIN OT TOO LITTLE GLUCOSE
  32. THE MAJOR DIABETIC COMPLICATION
    1EYES
    2HEART AND CORONARY CIRCULATION
    3KIDNEY
    4LOWER LIMBS
    5BRIAN AND CEREBRAL CIRCULATION
    6PERIPHERAL NERVOUS SYSTEM
    7DIABETIC FOOT
    • 1RETINOPATHY
    • 2CORONARY HEART DISEASE
    • 3NEPHROPATHY
    • 4PERIPHERAL VASCULAR DISEASE
    • 5CEREBROVASCULAR DISEASE
    • 6NEUROPATHY
    • 7ULCERATION AND AMPUTATION
  33. EFFECT ON BLOOD VESSELS
    • HIGH LEVEL OF GLUCOSE
    • PLAQUE IN ARTERY WALL
    • BLOOD CLOT
    • LEFT ANTERIOR DESCENDING ARTERY
    • RIGHT CORONARY ARTERY
  34. CHRONIC COMPLICATION MACROVASCULAR
    • CARDIOVASCULAR
    • HEARTDISEASE/MI
    • CEREBROVASCULAR
    • STROKE
    • DM PTS HAVE HEART DISEASE AND STROKE ROSKS 2 TO 4X HIGHER THAN NON- DM PTS
    • PERIPHERAL VASCULAR DISEASE
  35. CHRONIC COMPLICATION OF MICROVASCULAR
    • DIABETIC RETINOPATHY
    • NORMAL RETINA
    • MACULA OPTIC DISK
    • RATINOPATHY
    • HEMORRAGE ANEURYSMS


    THE LEADING CAUSE OF NEW CASES OF BLINDNESS IN ADULTS AGES 20-74
  36. CHRONIC COMPLICATION MICROVASCULAR
    • FOR MICROALBUMINURIA
    • GLIMERULUS
    • SCLEROTIC AFFERENT AND EFFERENT ARTERIOLES
    • SCLEROTIC RENAL ARTERY

    THE LEADING CAUSE OF ESRD OCCOUR IN ABOUT 20-40% OF PATIENTS WITH DIABETES
  37. DIABETIC NEUROPATHY MICROVASCULAR
    • Diabetic Neuropathy - the poor blood supply will cause the nervous system to malfunction
    • NERVES SHRIVEL WHEN BLOOD VESSELS DISAPPEAR
    • DUE DISEASE BLOOD VESSELS
  38. FOR DM PT FOOT
    • BLOOD VESSEL DAMAGE IN THE FEET MAY CAUSE TISSUE DAMAGE
    • GANGRENE
  39. MICROVASCULAR FOR SEXUAL PROBLEMS
    • SEXUAL PROBLEMS FOR MEN
    • EXECTILE DYSFUNCTION
    • Sexual problems for women
    • decreased vaginal lubrication
    • decreased sexual response
    • •Urologic problems for men and women
    • urinary tract infections neurogenic bladder
  40. MICROVASCULAR
    GASTROPARESIS
    NERVE DAMAGE TO THE DIGESTIVE SYSTEM MOST COMMONLY CAUSES CONSTIPATION. DAMAGE CAN ALSO CAUSE THE STOMACH TO EMPTY TOO SLOWLY
  41. METABOLIC SYNDROME
    • Metabolic Syndrome
    • Syndrome X
    • •Presence of metabolic factors that increase risk of developing DM 2 and CV disease
    • –Central obesity – apple shape (45 inches or more in men, 35 inches or more in women)
    • –Hyperglycemia
    • –HTN (> 130/85 mh/dL)
    • –Dyslipidemia
    • (Trig > 150 mg/dL; HDL < 40 mg/dL for men or < 50 mg/dL for women)
    • Teach re: ABC (A1c, Blood pressure, cholesterol control)
  42. MANAGEMENT OF DM
    • REGULAR BG MONITORING
    • SELF MONITORING BLOOD GLUCOSE(SMBG)
    • DRUG THERAPY
    • DIET
    • EXEERCISE
  43. GLYCEMIC DIET
    • FRUITS, VEG, COOKED OR DRESSED WOTH HEALTHFUL OIL)
    • REDUCED FAT DAIRY LEAN PROTEIN NUTS AND LEGUMES
    • UNREFINED GRAINS AND PASTA
    • REFINED GRAINS POTATO AND SWEETS
  44. DIET CONT
    GETTING THE BALANCE RIGHT
    • BIG PORTION FOR VEG AND FRUITS
    • PROTEIN
    • CANDY
  45. •Alcohol and DM
    • Can affect BG levels
    • Alcohol inhibits liver
    • glucose production
    • Potential for alcohol
    • induced hypoglycemia
  46. MANAGEMENT:EXERCISE
    • Helps regulate blood glucose
    • Increases insulin effectiveness and
    • sensitivity in the body.
    • Must monitor insulin and food intake to match
    • exercise regimen.
  47. ASSESSMENT TO DM
    • Check BG prior to administering any insulins or oral hypoglycemic agents
    • Monitorbefore meals and within 2 hours post prandial (PP)
    • Correction dose (with rapid or short acting insulins) given to treat blood glucose elevations
    • Common BG monitoring and correction dose frequency- (ACHS) but can be done more often
  48. DRUG THERAPY AND TYPE OF INSULIN
    • •Fast-acting insulin
    • –Rapid Acting Insulin Analogs
    • •Aspart, Lispro, Glulisin
    • –Regular Human Insulin
    • •Intermediate-acting insulin
    • –NPH Human Insulin
    • Novolin N/Relion N, Humulin N
    • –Pre-Mixed Insulin
    • Humulin 70/30, Humalog 75/25, etc.
    • •Long-acting insulin
    • Insulin Glargine, Insulin Detemir

    • BOLUS USED TO LOWER BLOOD SUGAR AFTER EATING A MEAL
    • BASAL USED TO LOWER BLOOD SUGAR THROUGHOUT THE DAY AND NIGHT
  49. •Drug Therapy Cont.: Insulin
    • Onset - how soon it starts to work in the blood
    • Peak - when the insulin has the greatest effect on blood sugar levels
    • Duration – how long it keeps working
    • Each insulin has its strengths and may be appropriate in different pt circumstances
  50. Drug Therapy-Insulin Cont:Rapid Acting Insulin Analogues “Logs”
    • Humalog (insulin lispro)
    • Novolog (insulin aspart)
    • Apidra (insulin glulisine)


    • •Bolus insulin
    • •Ideal for meal
    • coverage
  51. Drug Therapy-Insulin Cont:
    Short Acting: Regular
    Insulin regs
    • • Bolus insulin
    • Humulin R
    • NovolinR/ReliOn R
  52. Drug Therapy-Insulin
    Cont: Rapid Acting
    (Humalog/Novolog) VS.
    Short Acting (Regular Insulin)
    • rapid onset 15 min
    • peaks faster limited duration 3-5 h


    • short acting
    • delayed onset peaks in 2-4 hr
    • lasts 5-7 hours
  53. Drug Therapy-Insulin Cont:
    Intermediate acting:NPH Insulin
    • Basal insulin: covers blood sugar between
    • meals
    • Satisfies overnight insulin requirement
    • Need snack if NPH given at 5 pm (only)
    • Ideal to be given at 9 pm (HS) to address Dawn Phenomenon
    • 5 in morning growth hormone release that increase blood sugar
  54. hypoglycemia s/s
    hypoglycemia

    • H headache
    • I irritable/imparied vision
    • W weakness/fatigue
    • A anxious
    • Sshaking/sweating
    • H heartbeat
    • dizziness
  55. •Drug Therapy-Insulin Cont:Hypoglycemia
    •BS <60- 70 mg/dL

    • An acute complication
    • •Causes
    • •Tx:
    • (15/15 or 20/20 Rule)
    • Give 15/20 g simple carb and recheck BG in 15/20 minutes


    • 15g check in 15 min
    • 4oz oj and couple candy

    20g check in 20 min
  56. •Drug Therapy-Insulin Cont:L ong-Acting: Peakless Insulins!!!
    • Lantus (insulin glargine)
    • Levimir (insulin detimir)
    • •Basal Insulin
    • •No risk for hypoglycemia
    • •Do not mix with other insulins – becomes inactivated when mixed with other insulins

    • Peakless insulins are late
    • Lantus(glargine) and levimir(detimir)
    • When long acting insulin come out they try to gave at night. And 20-24 hour
    • coverage.
  57. AMYLIN
    • –A naturally occuring hormone secreted with insulin by
    • the beta cells
    • –action similar to insulin, responds to blood glucose elevation
    • –Amylin levels found to be decreased in DM type 1 pts

    • ANALIGUES
    • •Symlin: Synthetic analogue of human amylin

    • –Approved for use with insulin in adults with type 1 and type 2 diabetes
    • –Delays gastric emptying, reduces after meal BG levels, triggers sateity

    –Do not mix with insulin in one syringe
  58. INCRETIN HORMONE GLP-1
    • •Incretin hormone GLP-1
    • –Secreted once food is in the stomach
    • –Increases insulin secretion
    • –Inhibits glucagon secretion
    • –Slows the rate of gastric emptying
    • –Prevents hyperglycemia after meals
    • –Pts with DM2 found to have reduced incretin effect


    • •Byetta:Synthetic incretin(GLP-1) mimetic hormone
    • –Indicated for patients with type 2 diabetes who don’t use insulin
    • –Delays gastric emptying, slows nutrient absorption, reduces food intake (decreasing BG)
  59. •Insulin Administration
    • •Rotate injection site- prevents lipodystrophy
    • (hypertrophy and atrophy)
    • •Rotate within one anatomic site (rather than
    • from one site to another)
    • •Abdomen site- most rapid absorption



    • Atrphy loss of tone
    • Hypertrophy too much
    • Abdomen is most rapid site absorption
  60. DRUG THERAPY CONT: OTHER METHOD OF ADMINSITRATION
    • Insulin pump are used to controlled,
    • Disadvange

    • infection and site they have to change every
    • 2-3 day, but do body follow that
    • Pt use waterproof cover if they want to swimming
  61. •Drug Therapy Cont:Other Methods of Administration-Insulin pens
  62. •Small lightweight prefilled insulin cartridges
    • Dial insulin
    • Most accurate but expensive
  63. •Continuous IV insulin infusion
    • •Used to maintain glycemiccontrol in hospitalized patients with high blood glucose levels; in DKA and
    • HHNS
    • •Regular insulin may be used IV

    • •May also be given preoperatively or postoperatively
    • •More frequent BS monitoring ( q1-2 hours per agency protocol)

    Acute stage insulin gave as insulin drip for icu/ccu

    Continous drip
  64. •Oral Antidiabetic agents
    • •Oral Agents
    • –Modify insulin secretion
    • –Modify insulin sensitivity
    • –Modify glucose
    • absorption/secretion




  65. Sulfonylureas
    meglitinides
    • Sulfonylureas stimulate the pancreas to produce more insulin thesedrugs assist insulin in moving glucose into cell.
    • Drugs
    • acetphexamide

    Chlorpropamide (diabinese) glimepiride(amarly) glipizide(glucotrol) glyburide(micronase, diabeta)

    meglitinides

    No risk for hypoglycemina by metformin
  66. new oral med
    • januvia(sitagliptin) DPP INHINITOR
    • An oral drug that reduces blood sugar levels in patients with type 2 diabetes.
    • –DPP-4 increasesBG- its inhibition leads to
    • decreased BG
    • – Sitagliptin is the first approved member of
    • a class of drugs that inhibit the enzyme, dipeptidyl
    • peptidase-4 (DPP-4)
  67. DRUG THERAPY
    •BS <60- 70 mg/dL

    • •An acute complication
    • •Causes
    • •Tx:
    • (15/15 or 20/20 Rule)

    –Give 15/20 g simple and recheck BG in 15/20 minutes
  68. •Dawn phenomenon
    •Somogyieffect
    •Neuroglycopenic symptoms
    • Dawnphenomenon:high fasting blood sugar
    • level in the morning due unrecognized hypoglycaemic episode during the night in a person with diabetes due
    • to hormone
    • Somogyi effect Somogyieffect or chronicSomogyi rebound is a rebounding
    • high blood sugar that is a response to low blood sugar.[1] In context of
    • managing the blood glucose level manually with insulin injections, this effect
    • is counter-intuitive to insulin users who experience high blood sugar in the
    • morning as a result of an overabundance of insulin at night
    • Neuroglycopenic symptomsis a medical term that
    • refers to a shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia. Glycopenia affects the functionof neurons, and alters brain function and behavior. Prolonged neuroglycopenia can result in
    • permanent damage to the brain
  69. Diabetic TeachingNeeds
    • Disease process
    • S/S of hyperglycemia and hypoglycemia
    • Blood sugar monitoring
    • Diet
    • Exercise
    • Drug therapy
    • Sick Day Rules
    • Complications (acute and chronic)
    • Prevention: Foot care, eye exam etc.
  70. Preventionof Complications…
    Tight BS control

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