Care of the Client with Diabetes Mellitus: Type 1 and Type 2



Care of the Client with Diabetes Mellitus: Type 1 and Type 2

I. Terminology:

a. glycogenesis: promotion of the storage of glycogen when blood glucose levels are increased

b. glycogenolysis: breakdown of glycogen (stored carbohydrate) to glucose

c. glycolysis: the metabolism of glucose

d. lipolysis: the metabolism of fats and lipids

e. gluconeogenesis: process by which the liver synthesizes glucose from noncarbohydrate substances, especially proteins

f. polydipsia: excessive thirst

g. polyphagia: excessive appetite and eating

h. polyuria: excessive excretion of urine

i. hypoglycemia: Blood sugar < 70mg/dL

j. hyperglycemia: Blood sugar > 126 mg/dL

k. Type 1 DM: formerly known as insulin-dependent diabetes. Characterized by the destruction of pancreatic beta cells, usually leading to absolute insulin deficiency. Affects approximately 10% of people w/ diabetes and is usually diagnosed by the age of 30.

l. Type 2 DM: formerly known as noninsulin-dependent diabetes or adult-onset diabetes. Most common form of diabetes that affects 90-95% of people w/ diabetes. Usually diagnosed after the age of 40 yrs, but is becoming more common in younger people.

m. Impaired fasting glucose: People with Type 1 or 2 DM may be classified as having impaired glucose tolerance aka impaired fasting glucose: New diagnostic category defined by fasting glucose levels above 110 mg/dl but below 126 mg/dl.

II. Insulin Metabolism

1. Insulin is continuously released at a basal rate with increased rate when food is ingested.

2. Counterregulatory hormones stimulate glycogen release and breakdown the effect of insulin-e.g. norepinephrine and epinephrine both break down insulin. Other hormones that antagonize insulin:

1. growth hormone

2. cortisol

3. glucagon

3. This activity provides a steady but regulated release of glucose for energy during food intake.

III. Epidemiology of Diabetes Mellitus

1. Affects 18 million people or 8% of the population in the US

1. 9 million are undiagnosed

2. 9 million are diagnosed

□ Diabetes is the 7th leading cause of death in the US

□ By 2025, 1 in 3 or 4 Americans will have DM

□ Prevalence of DM by Race and Ethnicity

1. Pima Indians have 50% prevalence-causing them to have the highest rate of amputations and blindness

2. African Americans: have a 1.6 X rate of DM compared to Caucasians

3. Hispanic Americans are 2 X more likely compared to non-Hispanic Caucasians

4. Asians have a higher rate with Filipinos among the highest of the Asian population.

IV. Risk Factors for Diabetes Type 2

1. Obese (85%) of all people with Type 2 DM are obese.

2. + family member

3. Member of high risk population-e.g. race

4. Hypertensive

5. Dyslipidemic

6. Hx. of gestational DM or baby > 9 lbs.

7. Previous IGT or IPG: (Impaired glucose tolerance/prediabetes/ BS btw. 110-126 mg/dl) IPG: Impaired plasma glucose

V. Etiology of Type 1 DM

1. Development of Type 1 DM broken down into 5 stages

1. genetic predisposition

2. environmental trigger

3. active autoimmunity

4. progressive beta cell destruction

5. overt diabetes mellitus

2. Genetic Predisposition:recessive gene + autoimmune response can destroy

islet cells on the pancreas

3. Type 1 DM does not develop in all people who have a genetic predisposition

4. Autoimmune disorder

VI. Etiology/Pathophysiology of Type 2 DM

1. Decreased tissue responsiveness to insulin as a result of receptor site defects: means that very little or not enough insulin is getting into the cells.

2. Increased/Overproduction of insulin occurs early on but islet/beta cells are eventually exhausted/worn out. Insulin exhaustion

3. Abnormal hepatic glucose production = liver is releasing glucose at the wrong times due to unknown etiology

VII. Classification of DM

1. Type 1:

1. Usually young, thin with abrupt signs and symptoms such as polyuria, polyphagia, polydipsia

2. Increased genetic susceptibility

3. Multiple islet cell antibodies (ICAs)-test is done to assess for presence of antibodies

4. Absolutely no insulin production as islet cells have been destroyed

5. Usually diagnosed/found in ketosis (ketosis: the accumulation of ketones caused by rapid oxidation of fatty acids)

□ Type 2:

1. Usually >35 years old (although more kids are now diagnosed with Type 2 DM)

2. Insidious onset (no clear symptoms initially)

3. Obesity, lack of exercise

4. Genetic susceptibility

5. Relative insulin production (some insulin produced by the pancreas)

6. No islet cell antibodies (islet cells are not being destroyed by antibodies with Type2)

7. Usually not found in ketosis

□ Prediabetes:

1. Fasting glucose levels >100 mg/dl but less than 126 mg/dl

VIII. Clinical Manifestations

|Type 1 Diabetes Mellitus |Type 2 Diabetes Mellitus |

|Abrupt Onset |Insidious Onset |

|S&S: |S&S: |

| Polyuria | Polyuria |

| Polyphagia | Polyphagia |

| Polydipsia | Polydipsia |

| Fatigue | Fatigue |

|Weight Loss |Wounds that do not heal (Increased risk |

| |of amputations) |

| |Impotence |

| |Blurred Vision |

| |Vaginal infections/fungal infections of toes |

IX. Diagnostic Studies:

1. Screen should be considered >45 yrs of age and at 3 yr. intervals b/c incidence increases @ 45 yrs.

2. Symptoms + casual /random glucose >200 mg/dl

random test taken at any time of day without regard to time since last meal. If >200 mg/dl plus S&S such as polyuria, polydipsia and/or unexplained weight loss = diagnosis for DM

3. Fasting plasma glucose > 126 mg/dl = diagnosis of DM.

normal value is 140 mg/dl (according to blackboard slides)

2 hours following a meal, blood is drawn. Glucose levels >200 mg/dl (according to Text) is an indication to diagnose DM. Glucose levels btw 140-200= diagnosis of impaired glucose tolerance. Normal levels: 80-140 mg/dl.

5. Glycosylated hemoglobin or A1C ................
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