Diabetes Mellitus type 1 Dr. Mahtab Ordooei spring 2015.
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Transcript of Diabetes Mellitus type 1 Dr. Mahtab Ordooei spring 2015.
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Diabetes Mellitus type 1
Dr. Mahtab Ordooeispring 2015
Diabetes Mellitus type 1
Dr. Mahtab Ordooeispring 2015
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Diabetes MellitusDefinition
Diabetes MellitusDefinition
• A multisystem disease related to:
– Abnormal insulin production, or
– Impaired insulin utilization, or
– Both of the above
• Leading cause of heart disease, stroke, adult blindness, and non-traumatic lower limb amputations
• A multisystem disease related to:
– Abnormal insulin production, or
– Impaired insulin utilization, or
– Both of the above
• Leading cause of heart disease, stroke, adult blindness, and non-traumatic lower limb amputations
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Normal Insulin MetabolismNormal Insulin Metabolism
• Insulin
– Produced by the cells in the islets of Langherans of the pancreas
– Facilitates normal glucose range of 3.9 – 6.7 mmol/L
• Insulin
– Produced by the cells in the islets of Langherans of the pancreas
– Facilitates normal glucose range of 3.9 – 6.7 mmol/L
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Insulin SecretionInsulin Secretion
Fig. 47-1
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Normal Insulin MetabolismNormal Insulin Metabolism
• Promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell
• Analogous to a “key” that unlocks the cell door to allow glucose in
• Promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell
• Analogous to a “key” that unlocks the cell door to allow glucose in
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Normal Insulin Metabolism Normal Insulin Metabolism
Insulin after a meal:• Stimulates storage of glucose as
glycogen
• Inhibits gluconeogenesis
• Enhances fat deposition in adipose tissue
• Increases protein synthesis
Insulin after a meal:• Stimulates storage of glucose as
glycogen
• Inhibits gluconeogenesis
• Enhances fat deposition in adipose tissue
• Increases protein synthesis
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Normal Insulin Metabolism
• Fasting state– Counter-regulatory hormones (especially
glucagon) stimulate glycogen glucose
• When glucose unavailable during fasting state– Lipolysis (fat breakdown) – Proteolysis (amino acid breakdown)
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Type 1 Diabetes MellitusType 1 Diabetes Mellitus
• Formerly known as “juvenile onset” or “insulin dependent” diabetes
• Most often occurs in people under 30 years of age
• Peak onset between ages 11 and 13
• Formerly known as “juvenile onset” or “insulin dependent” diabetes
• Most often occurs in people under 30 years of age
• Peak onset between ages 11 and 13
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Type 1 Diabetes MellitusEtiology and PathophysiologyType 1 Diabetes Mellitus
Etiology and Pathophysiology
• Progressive destruction of pancreatic cells
• Autoantibodies cause a reduction of 80% to 90% of normal cell function before manifestations occur
• Progressive destruction of pancreatic cells
• Autoantibodies cause a reduction of 80% to 90% of normal cell function before manifestations occur
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Type 1 Diabetes MellitusEtiology and PathophysiologyType 1 Diabetes Mellitus
Etiology and Pathophysiology
• Causes:
– Genetic predisposition
– Exposure to a virus
• Causes:
– Genetic predisposition
– Exposure to a virus
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Type 1 Diabetes MellitusOnset of Disease
Type 1 Diabetes MellitusOnset of Disease
• Manifestations develop when the pancreas can no longer produce insulin
– Rapid onset of symptoms
– Present at ER with impending or actual ketoacidosis
• Manifestations develop when the pancreas can no longer produce insulin
– Rapid onset of symptoms
– Present at ER with impending or actual ketoacidosis
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Type 1 Diabetes MellitusOnset of Disease
Type 1 Diabetes MellitusOnset of Disease
• Weight loss
• Polydipsia (excessive thirst)
• Polyuria (frequent urination)
• Polyphagia (excessive hunger)
• Weakness and fatigue
• Ketoacidosis
• Weight loss
• Polydipsia (excessive thirst)
• Polyuria (frequent urination)
• Polyphagia (excessive hunger)
• Weakness and fatigue
• Ketoacidosis
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Type 1 Diabetes MellitusOnset of Disease
Type 1 Diabetes MellitusOnset of Disease
• Diabetic ketoacidosis (DKA)
– Life-threatening complication of Type 1 DM
– Occurs in the absence of insulin
– Results in metabolic acidosis
• Diabetic ketoacidosis (DKA)
– Life-threatening complication of Type 1 DM
– Occurs in the absence of insulin
– Results in metabolic acidosis
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Clinical ManifestationsType 1 Diabetes MellitusClinical ManifestationsType 1 Diabetes Mellitus
• Polyuria
• Polydipsia
• Polyphagia
• Weight loss
• Polyuria
• Polydipsia
• Polyphagia
• Weight loss
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Diabetes MellitusDrug Therapy: Insulin
Diabetes MellitusDrug Therapy: Insulin
• Exogenous insulin:
– Required for all patient with type 1 DM
– Prescribed for the patient with type 2 DM who cannot control blood glucose by other means
• Exogenous insulin:
– Required for all patient with type 1 DM
– Prescribed for the patient with type 2 DM who cannot control blood glucose by other means
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Diabetes MellitusDrug Therapy: Insulin
Diabetes MellitusDrug Therapy: Insulin
• Types of insulin
– Human insulin
• Most widely used type of insulin
• Cost-effective Likelihood of allergic reaction
• Types of insulin
– Human insulin
• Most widely used type of insulin
• Cost-effective Likelihood of allergic reaction
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Diabetes MellitusDrug Therapy: Insulin
Diabetes MellitusDrug Therapy: Insulin
• Types of insulin
– Insulins differ in regard to onset, peak action, and duration
– Different types of insulin may be used for combination therapy
• Types of insulin
– Insulins differ in regard to onset, peak action, and duration
– Different types of insulin may be used for combination therapy
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Insulin PreparationsInsulin Preparations
Fig. 47-3
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Diabetes MellitusDrug Therapy: Insulin
Diabetes MellitusDrug Therapy: Insulin
• Types of insulin
– Rapid-acting: Lispro
– *Short-acting: Regular
– *Intermediate-acting: NPH or Lente
– Long-acting: Ultralente, Lantus
• Types of insulin
– Rapid-acting: Lispro
– *Short-acting: Regular
– *Intermediate-acting: NPH or Lente
– Long-acting: Ultralente, Lantus
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4:00 16:00 20:00 24:00 4:00
Breakfast Lunch Dinner
Insu
lin
Acti
on
8:0012:008:00Time
REG REG NPH/LenteNPH/Lente
Twice-Daily Split-Mixed Regimen
Adapted with permission from Leahy J. In: Leahy J, Cefalu W, eds. Insulin Therapy. New York: Marcel Dekker; 2002:87; Nathan DM. N Engl J Med. 2002;347:1342
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4:004:00 16:0016:00 20:00 20:00 24:0024:00 4:004:00
BreakfastBreakfast LunchLunch DinnerDinner
8:008:0012:0012:008:008:00
TimeTime
Glargine
Basal/Bolus Treatment Program WithRapid- and Long-Acting Analogs
Insu
lin
Act
ion
Adapted with permission from Leahy JL. In: Leahy J, Cefalu W, eds. Insulin Therapy. New York: Marcel Dekker Inc.; 2002:87; Nathan DM. N Engl J Med. 2002;347:1342
Aspart or
Lispro
Aspart or
Lispro
Aspart or
Lispro
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Diabetes MellitusDrug Therapy: Insulin
Diabetes MellitusDrug Therapy: Insulin
• Insulin
– Cannot be taken orally
– Self-administered by SQ injection
• Insulin
– Cannot be taken orally
– Self-administered by SQ injection
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Injection SitesInjection Sites
Fig. 47-5
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Diabetes MellitusDrug Therapy: Insulin
• Insulin delivery methods– Ordinary SQ injection– Insulin pen
• preloaded with insulin; “dial” the dose
– Insulin pump• Continuous “basal” infusion. At mealtime, user
programs to deliver “bolus” infusion that correlates with amount of CHOs ingested. Allows tight control and greater flexibility with meals and activity
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Diabetes MellitusDrug Therapy: Insulin
• Insulin delivery methods– Intensive insulin therapy
• Multiple daily injects and frequent SMBG
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Diabetes MellitusDrug Therapy: Insulin
Diabetes MellitusDrug Therapy: Insulin
• Problems with insulin therapy– Hypoglycemia (BS < 3.9 mmol/L)
• Due to too much insulin in relation to glucose availability
• Problems with insulin therapy– Hypoglycemia (BS < 3.9 mmol/L)
• Due to too much insulin in relation to glucose availability
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Diabetes MellitusDrug Therapy: Insulin
• Problems with insulin therapy– Hypoglycemia– Allergic reactions
• Local inflammatory reaction
– Lipodystrophy• Hypertrophy or atrophy of SQ tissue r/t frequent
use of same injection site. Less common now b/c pork and beef insulin infrequently used
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Diabetes MellitusDrug Therapy: Insulin
• Problems with insulin therapy– Somogyi effect
• Due to too much insulin• Early morning hypoglycemia followed by
hyperglycemia (d/t stimulation of counter-regulatory hormones)
– Dawn Phenomenon• Hyperglycemia secondary to nighttime release of
growth hormone (a counter-regulatory hormone) that cause BS in early am (5 – 6 am).
• Rx with insulin that will peak at that time (intermediate at 10 pm)
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Diabetes MellitusPancreas Transplantation
Diabetes MellitusPancreas Transplantation
• Used for patients with type 1 DM who have end-stage renal disease and who have had or plan to have a kidney transplant
• Eliminates the need for exogenous insulin
• Can also eliminate hypoglycemia and hyperglycemia
• Used for patients with type 1 DM who have end-stage renal disease and who have had or plan to have a kidney transplant
• Eliminates the need for exogenous insulin
• Can also eliminate hypoglycemia and hyperglycemia
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Diabetes Mellitus Acute Complication : Hypoglycemia
• Hypoglycemia– Too much insulin (or oral agents) in relation
to glucose availability– Usually coincides with peak action of
insulin/OA
• Brain requires constant glucose supply thus hypoglycemia affects mental function
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Diabetes Mellitus Acute Complication : Hypoglycemia
• S/S hypoglycemia– S/S of brain glucose deprivation (CNS symptoms)
• Confusion, irritability– S/S of SNS stimulation (anxiety, tachycardia, tremors)– Diaphoreses, tremor, hunger, weakness, visual
disturbances– If untreated → LOC, seizures, coma, death
• Hypoglycemic unawareness– autonomic neuropathy interferes with counter-
regulatory hormones– Patients on β-blockers
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Diabetes Mellitus Acute Complication : Hypoglycemia
• Treatment for hypoglycemia– Ingest simple CHO (fruit juice, soft drink),
or commercial gel or tablet– Avoid sweets with fat (slows sugar absorption)
– Repeat Q15min until < 3.9 mmol/L– Then eat usual meal snack or meal and
recheck
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Diabetes Mellitus Acute Complication : Hypoglycemia
• Treatment for hypoglycemia if not alert enough to swallow– Glucagon 1m IM or SQ (glycogen → glucose)
– Then complex CHO when alert
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Diabetes Mellitus Acute Complication : DKA
• Diabetic Ketoacidosis (DKA): BG > 20 – 30 mmol/L– Usually in Type 1 diabetes; can occur in
Type 2– Causes:
• Infection**• Stressors (physiological, psychological) • Stopping insulin• Undiagnosed diabetes
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Diabetes MellitusAcute Complication: DKA
• Pathophysiology– Continuation of effects of insulin deficiency
• Severe metabolic acidosis• Severe dehydration → shock• Severe electrolyte imbalance ( ↓ Na, ↓ K, ↓ Cl, ↓ Mg, ↓ PO4)
• Clinical Manifestations– S/S dehydration ( HR; BP, poor turgor, dry MM), – Kussmauls breathing (d/t metabolic acidosis)– Fruity breath (d/t acetone)– Abdominal pain, N & V, cardiac dysrhythmias
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Diabetes MellitusAcute Complication: DKA
• Treatment– Replace fluid and electrolytes – Insulin (First IV bolus, then infusion)– ID and correct precipitating cause (e.g.,
infection, etc.) – Teaching re: diabetes control