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NUR 202 Week 3 > Diabetes Pt 1 > Flashcards

Diabetes Pt 1 Flashcards

1
Q

Diabetes Mellitus (DM)

  • A chronic, multisystem dz r/t abn insulin production, impaired insulin utilization, or both
  • Affects 25.8 million people (8.3% of population)
  • 7th leading cause of death
A
  • Leading cause of
    > adult blindness
    > end-stage kidney dz
    > nontraumatic lower limb amputations
  • Major contributing factor
    > heart dz (2-4x)
    > stroke (2-4x)
    > HTN (67% of those w/)
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2
Q

Etiology & Pathophysiology

  • Singly or in combination of causative factors
    > genetic
    > autoimmune
    > environmental (e.g., viruses, obesity)
  • A disorder of glucose metabolism r/t absent or insufficient insulin supply and/or poor utilization of insulin that’s avail
A

Classes of Diabetes

  • Type 1*
  • Type 2*
  • Gestational
  • Other specific types (d/t various causes)

(*) = most common

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3
Q

Type 1

Formerly juvenile-onset or insulin-dependent diabetes (IDDM); 5% of all cases

  • Affects those <40 y.o. & 40% develop before age 20
  • Happening more in young children
A
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4
Q

Type 2 Diabetes Mellitus

  • Formerly known as adult-onset diabetes (AODM) or non-insulin-dependent diabetes (NIDDM)

! Most prevalent type (90-95%)

  • Risk factors: overweight, obesity, advancing age, fhx
  • Incr incidence in children d/t incr in prevalence of childhood obesity
  • Greater prevalence in ethnic groups
  • African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, & Native Americans than whites
A

Type 2 DM - Etiology & Pathophysiology

  • Pancreas continues to produce some endogenous (self-made) insulin
  • Insulin insufficient, poorly utilized, or both
  • Multiple etiologic factors
    > Obesity is greatest risk factor (esp abdominal & visceral adiposity)
    > Genetic component increases insulin resistance & obesity
  • Individuals w/a 1st degree relative w/the dz are 10x more likely to develop Type 2 DM
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5
Q

The presence of endogenous insulin is a major distinction between type 1 & type 2 DM; in type 1 there is an absence of endogenous insulin

A

4 major metabolic abnormalities

  1. Insulin resistance
  2. Decreased insulin production by pancreas
  3. Inappropriate hepatic glucose production
  4. Altered production of hormones & cytokines by adipose tissue (adipokines)
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6
Q

Insulin resistance

  • Body tissues aren’t responding to action of insulin and/or insufficient in #
  • Most insulin receptors located on skeletal muscle, fat, & liver cells
  • When insulin not properly used, entry of glucose into cell is impeded, resulting in hyperglycemia
A
  • In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amts of insulin (if β-cell function is normal)
    > This creates a temporary state of hyperinsulinemia that coexists w/hyperglycemia
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7
Q

Decreased insulin production by pancreas

  • As β-cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost
  • Underlying reason why β-cells fail to adapt is unknown
A
  • May be linked to adv effects of chronic hyperglycemia or high levels of circulating free fatty acids
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8
Q

Inappropriate glucose production by the liver

  • I/o properly regulating the release of glucose in response to blood lvls, liver does so in a haphazard way that doesn’t correspond to the body’s needs @ the time

! But, this isn’t considered a primary factor in the development of type 2 DM

A
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9
Q

Altered production of hormones & cytokines by adipose tissue (adipokines)

  • Adipokines secreted by adipose tissue appear to play a role in glucose & fat metabolism & are likely to contribute to the pathophysiology of type 2 DM
  • Adipokines are thought to cause chronic inflammation, a factor involved in insulin resistance, type 2 DM, & cardiovascular dz

What are the 2 adipokines thought to affect insulin sensitivity?

A

adiponectin, leptin

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10
Q

____ increases risk for type 2 DM
- elevated glucose lvls
- abdominal obesity
- elevated BP
- high lvls of triglycerides
- decreased lvls of HDLs

A

Metabolic syndrome

3/5 sx’s = considered to have ↑

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11
Q

Type 2 DM: Onset of Disease

  • Gradual onset
  • Hyperglycemia may go many years w/o being detected
  • Many times discovered w/routine lab testing
A

> Find an elevated glucose or Hgb A1C

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12
Q

Prediabetes

  • Individuals at risk for type 2 DM
  • Is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both
A
  • It’s an intermediate stage between normal glucose homeostasis & DM in which the blood glucose lvls are elevated but not high enough to meet the diagnostic criteria for diabetes
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13
Q

A diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are ___-___ mg/dL

A

140-199 mg/dL

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14
Q

Impaired fasting glucose (IFG) is diagnosed when fasting blood glucose lvls are ___-___ mg/dL

A

100-125 mg/dL

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15
Q
  • Asymptomatic, but long-term damage already occurring (esp to heart & blood vessels)
  • Pt teaching important
    > Undergo screening
    > Manage risk factors
    > Monitor for sx’s of DM
    > Maintain healthy wt, exercise, healthy diet
A
  • Maintaining a healthy wt, exercising regularly, & eating a healthy diet have all been found to reduce the risk of developing overt DM in people w/prediabetes
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16
Q

Type 1 DM: Clinical Manifestations

Classic symptoms
* Polyuria (frequent urination)
* Polydipsia (excessive thirst)
> these 2 signs d/t the osmotic effect of glucose
* Polyphagia (excessive hunger)
> a consequence of cellular malnourishment when insulin deficiency prevents use of glucose for energy

A
  • Wt loss
    > may occur b/c the body cannot get glucose & turns to other energy sources, like fat & protein
  • Weakness, fatigue
    > b/c body cells lack needed energy from glucose
  • Ketone bodies
  • Hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion, & hypoxia
  • Acidosis, Kussmaul respirations
17
Q

Type 2 DM: Clinical Manifestations

  • Nonspecific sx’s (classic sx’s of type 1 may manifest)
    > Fatigue
    > Recurrent infections
    > Recurrent vaginal yeast or candidal infection
    > Prolonged wound healing
    > Visual changes
A
18
Q

Absence of Insulin

  • Hyperglycemia
  • Polyuria, polydipsia, polyphagia
  • Ketone bodies
  • Hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion, & hypoxia
  • Acidosis, Kussmaul respiration
A

Although you might see vague differences in the symptoms between Type 1 and Type 2, ultimately, it’s the absence of insulin that causes all of them & this is what ends up happening

19
Q

Diagnostic Studies

  1. Hemoglobin A1C level of ___% or higher
A

6.5%

20
Q
  1. Fasting plasma glucose (FPG) level higher than ___mg/dL

(Fasting as no caloric intake for at least 8 hrs)

A

126

21
Q
  1. Two-hour plasma glucose level during OGTT: ___mg/dL (with glucose load of 75g)
A

200

22
Q
  1. Classic symptoms of hyperglycemia with random plasma glucose level of ___mg/dL or higher
A

200

23
Q

If a patient presents w/a hyperglycemic crisis or clear sx’s of hyperglycemia (polyuria, polydipsia, polyphagia) w/a random plasma glucose level of 200 or higher, repeat testing is not warranted

  • Otherwise, criteria 1 through 3 should be confirmed by repeat testing to r/o lab error. It’s preferable for the repeat test to be the same test used initially. e.g., if a random blood glucose test showed elevated blood glucose levels, the same test should be used again when retesting
A
  • The accuracy of test results depends on adequate pt prep & attention to the many factors that may influence the test results. e.g., factors that can cause falsely elevated values include recent severe restrictions of dietary carbs, acute illness, medications (e.g., contraceptives, corticosteroids), & restricted activity like bed rest
  • A pt w/impaired GI absorption or who has recently taken acetaminophen may have false-negative test results
24
Q

Hemoglobin A1C test

  • Glycosylated Hgb: reflects glucose levels over past 2-3 mos
  • Used to diagnose, monitor response to therapy, & screen pts w/prediabetes
  • Goal: Normal Adult Range 4-6%
    > 5.7-6.4% = increased risk for DM
    > ADA (2014) defines levels >___% as diagnostic of DM
A

6.5

25
Q
  • The Hgb A1C test has several advantages over the FPG test, including greater convenience b/c fasting is not req’d
  • Dz’s affecting RBC’s (e.g., iron def anemia or sickle cell anemia) can influence the Hgb A1C lvl & should be considered in interpreting test results
A
  • The ADA identifies a Hgb A1C goal for pts with DM of less than 7.0%; normal range is considered 4-6%
26
Q

?

Can also be used to assess glucose control

  • Is formed by a chemical rxn of glucose w/plasma protein & reflects glucose control in the previous 1-3 wks
  • Lvls may show a change in glucose control before Hgb A1C does
A

Fructosamine

27
Q

Islet cell autoantibody testing is ordered primarily to help distinguish between autoimmune type 1 DM & DM d/t other causes

A

Collaborative Care

Goals of diabetes management
- Decrease sx’s
- Promote well-being
- Prevent acute complications
- Delay onset & progression of long-term complications

Need to maintain blood glucose levels as near to normal as possible

28
Q

Patient teaching
- Nutritional therapy
- Drug therapy
- Exercise
- Self-monitoring of blood glucose

Diet, exercise, & weight loss may be sufficient for pts w/type 2 DM

All pts w/type 1 require insulin

A

The major types of glucose-lowering agents (GLAs) used in the treatment of DM are insulin, oral agents (OAs), & noninsulin injectable agents

NUR 202 Week 3 (7 decks)

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