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Nursing 172 > Week 10: Chp 44: Type 1 Diabetes > Flashcards

Week 10: Chp 44: Type 1 Diabetes Flashcards

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1
Q

Risk Factors in the development of Type 1 diabetes

A
  • family history
  • autoimmune disorders (autoimmune thyroid disease, celiac disease, or Addison’s disease)
  • Environmental triggers in genetically sensitive individuals
  • Triggers as in viruses such as mumps, rubella, and Coxsackie B4; toxic chemicals; exposure to cow’s milk with the development of bovine antibodies; and cytotoxins (substances that are toxic to and kill living cells)
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2
Q

Type 1 Diabetes is typically triggered by what?

A

an autoimmune process in which the insulin-producing beta cells of the pancreas are destroyed, resulting in absolute lack of insulin

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3
Q

What will Type 1 Diabetes require?

A

-life-long insulin

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4
Q

Clinical Manifestations of Type 1 diabetes are caused by what?`

A

caused by hyperglycemia

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5
Q

Clinical Manifestations of Type 1 Diabetes Include?

A

polyuria, polydipsia, polyphagia, fatigue, and weight loss

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6
Q

Why does polyuria happen?

A

polyuria is increased volumes of urine, which is due to an increased concentration of glucose in the urine (glucosuria)
-hyperglycemia results in glucose excretion in the urine

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7
Q

Glucosuria

A

increased concentration of glucose in the urine

-this is why a patient experiences polyuria

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8
Q

Where is glucose usually reabsorbed?

A

in the renal tubules
-hyperglycemia results in glucose excretion in the urine, which creates an osmotic effect that effectively reduces water reabsorption into the renal tubules, leading to excessive volume loss through the kidneys

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9
Q

Why does polydipsia happen?

A

hyperglycemia also causes hyperosmolality in the blood, which causes a shift of fluid from the intracellular space to the vascular space
-the loss of intracellular water combined with the volume loss through the kidneys creates excessive thirst

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10
Q

Why does polyphagia happen?

A

the lack of insulin necessary to move glucose into the cells leads to the breakdown of protein and fat as a source of energy

  • this starvation of the cells leads to polyphagia, increased appetite
  • despite an increased appetite leading to consumption of large amounts of food, the continual breakdown of fats and protein leads to weight loss and fatigue
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11
Q 
Connection Check: The nurse monitors for which clinical manifestations in the patient newly diagnosed with Type 1 Diabetes? Select all that apply
A. Polyuria
B. Fatigue
C. Weight loss 
D. Polyphagia
E. Decreased appetite
A

A, B, C, and D
-a person with Type 1 diabetes have an increased appetite because of the starvation of the cells that lack the breakdown of glucose for energy

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12
Q

How is Type 1 Diabetes Diagnosed?

A
  • Hemoglobin A1c Test
  • Fasting blood glucose
  • 2-hr postprandial or the oral glucose tolerance test (OGTT)
  • random blood glucose
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13
Q

Hemoglobin A1c Test

A

measures the average blood glucose concentration over time by measuring the amount of glucose that binds to red blood cells (RBCs)

  • the test gives an accurate indication of long-term, time-averaged glucose levels over 6 to 12 weeks prior to the HgbA1c blood draw
  • when blood glucose concentration are high, more hemoglobin is affected
  • greater than or equal to 6.5% = DM
  • 5.7%-6.4% = prediabetes
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14
Q

Why is the Hemoglobin A1c test a good tool to monitoring the effectiveness of insulin therapy?

A

on the day of the HgbA1c sample, eating, physical activity, or acute stress do not affect the result, and the test can be done at any time of day and does not require fasting

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15
Q

When is Hemoglobin A1c tests not accurate

A

in several clinical situations, such as recent blood loss or transfusions; in the setting of anemia and treatment with erythropoietin (RBCs) which are common in patients with diabetic renal disease
-measurement depends on RBC survival and the composition of RBC hemoglobin

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16
Q

Fasting Blood Glucose

A

includes no caloric intake for at least 8 hours

  • without adequate oral intake, glucagon is released from the pancreas, facilitating the release of glycogen stores from the liver and increasing circulating blood glucose levels
  • without adequate insulin, hyperglycemia results
  • greater than or equal to 126 mg/dL = DM
  • 100-125 mg/dL = prediabetes
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17
Q

2 hr postprandial (after meals)/ Oral glucose tolerance test (OGTT)

A

test is performed by asking the patient to consume a beverage containing a glucose load, the equivalent of 75 g of carbohydrate, after fasting for 8 to 12 hours.

  • blood samples are taken prior to consuming the drink to get a fasting level, then again at 1 hour and 2 hours after consumption
  • the diagnostic value is based on the blood glucose level 2 hours after consumption
  • level greater than or equal to 200 mg/dL = DM
  • 140-199 mg/dL = prediabetes
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18
Q

Random Blood Glucose

A

level of greater than or equal to 200 mg/dL in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis may be indicative of diabetes mellitus

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19
Q

Connection Check: The nurse correlates which laboratory value with the diagnosis of DM?
A. Fasting blood glucose greater than 140 mg/dL
B. Hemoglobin A1c 5.8%
C. Random Blood Glucose 150 mg/dL
D. OGTT 155 mg/dL

A

A fasting blood glucose greater than 140 mg/dL

-greater than or equal to 126 mg/dL from a fasting blood glucose test is indicative of DM

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20
Q

Successful Treatment strategies for Type 1 Diabetes

A

-pharmacological interventions, nutrition management, patient education, and self-management

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21
Q

What is the primary pharmacological intervention?

A

insulin administers subcutaneously

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22
Q

The goal of treatment

A

to maximize glycemic control, the maintenance of blood glucose levels within normal ranges, in an effort to prevent the complications of hyperglycemia

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23
Q

Why don’t we give oral insulin administration for someone with Type 1 diabetes?

A

oral administration of insulin is not effective because it is broken down and rendered ineffective during the digestive process

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24
Q

Why is Insulin Considered a Safety alert?

A

insulin is a high-risk medication with a narrow therapeutic margin

  • tight glycemic control increases the risk of hypoglycemia in patients who rely on insulin and oral agents that stimulate the release of insulin to manage their diabetes; the benefits of tighter glucose control may not outweigh the risks for some patients; this includes patients with a limited life expectancy, those with comorbidities where a hypoglycemic event will have more serious consequences, or those unwilling or unable to do the monitoring necessary to prevent hypoglycemia
  • this risk is especially pronounced in patients with a tendency toward hypoglycemia, such as older adults, the malnourished, or those with renal or liver disease
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25
Q

What is most effective in maintaining tight glycemic control?

A

approach using a combination of long-acting or intermediate acting insulin once or twice a day to provide basal insulin
-these include rapid-acting and short-acting insulin taken at mealtimes to cover the incoming carbohydrates, prandial insulin or nutritional insulin, and a “sliding scale” of additional supplemental or correctional insulin to compensate for blood glucose elevations

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26
Q

How to determine when to use correctional insulin

A

the need for correctional insulin is determined by a random blood glucose level done via fingerstick immediately prior to eating

  • the prandial and correctional insulins are then administered at the same time prior to eating
  • in hospitalized patients with questionable or minimal oral intake, prandial and correctional insulins can be given immediately after the meal to confirm adequate carbohydrate intake
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27
Q

Insulin can be provided subcutaneously using what approaches?

A
  • Drawn up from a vial and administered via needle and syringe
  • insulin pen
  • insulin pump
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28
Q

Most typical insulin concentration syringe

A

U-100

-100 units of insulin per millimeter

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29
Q

U-100 insulin syringes come in several sizes

A

-1 mL that holds 100 units
-0.5 mL that holds 50 units
-0.3 that holds 30 units
> the patient should choose the insulin syringe size according to his or her insulin dosage

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30
Q

What syringe is used if there is a patient with insulin requirements being massive but of extreme insulin resistance?

A

a U-500 insulin concentration is available but by special order

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31
Q

Insulin Pen

A

allows the patient to dial in the exact dosage, avoiding the potential errors inherent in measuring and drawing up insulin in a traditional way
-consists of a injection button, dosage knob, dose window, and insulin cartridge

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32
Q

Insulin Pump

A
  • continuous subcutaneous insulin provided by a computer-driven device that delivers insulin according to instructions programmed by the patient
  • more convenient and able to deliver precise doses
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33
Q

Complications that come with the use of an Insulin pump

A
  • the demands of the pump therapy, self-consciousness in wearing the pump, fear of pump failure, and hypoglycemia
  • more disadvantages are the expense, the need for active participation and learning by the patient in response to glucose levels, the need to “wear” the pump continuously, skin issues around the insertion site, and potential complications if the pump malfunctions
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34
Q

Rapid Acting Prandial Insulin

A
  • rapid acting
  • used within 0-15 minutes prior to eating or used as correction insulin for blood glucose elevations; used in combination with long-acting insulin
  • Drugs: Lispro (Humalog) , Aspart (NovoLog) , Glulisine (Apidra)
35
Q

Rapid Acting Prandial Insulin: Lispro (Humalog)

A 
Onset: 15-30 minutes
Peak: 30-90 minutes
Duration: 3-5 hours
Purpose: also available in U-200 concentrated forms for people requiring larger doses
-rapid acting
36
Q

Rapid Acting Prandial Insulin: Aspart (NovoLog)

A

Onset: 10-20 minutes
Peak: 40-50 minutes
Duration: 3-5 hours
-rapid acting

37
Q

Rapid Acting Prandial Insulin: Glulisine (Apidra)

A

Onset: 20-30 minutes
Peak: 30-60 minutes
Duration: 1-2.5 hours
-rapid acting

38
Q

Short Acting Prandial Insulin

A

prandial insulin used for meals eaten within 30 to 60 minutes after administration; used in combination with long-acting insulin
Drugs: Regular Humulin R/ Novolin

39
Q

Short Acting Prandial Insulin: Regular Humulin R/ Novolin

A

Onset: 30-60 minutes
Peak: 2-5 hours
Duration: 5-8 hours

40
Q

Intermediate-acting Insulin

A

covers insulin needs for approximately half the day or overnight; used in combination with rapid-acting or short-acting insulin
Drug: NPH

41
Q

Intermediate-acting insulin: NPH

A

Onset: 1-2 hours
Peak: 4-12 hours
Durations: 18-24 hours

42
Q

Long- Acting Insulin

A

basal insulin; used in combination with rapid-acting or short-acting insulin
-Drugs: Glargine (Lantus), Detemir (Levemir)

43
Q

Long-acting insulin: Glargine (Lantus)

A

basal insulin
Onset: 1-1.5 hours
Peak: no peaks or valleys
Duration: 20-24 hours

44
Q

Long-Acting Insulin: Detemir (Levemir)

A

basal insulin
Onset: 1-2 hours
Peak: no peaks or valleys
Duration: 24 hours

45
Q

Complications

A
  • diabetic ketoacidosis (DKA)
  • hypoglycemia
  • dawn phenomenon and Somogyi effect
46
Q

Complications: Diabetic Ketoacidosis

A

there is inadequate insulin for cells to obtain adequate glucose for normal metabolism

  • the body attempts to obtain energy by the rapid breakdown of fat stores, releasing fatty acids from adipose tissue; the liver converts the fatty acids into ketone bodies, which can serve as an energy source in the absence of glucose; the ketone bodies have a low pH, resulting in metabolic acidosis
  • the absence of insulin also results in an increased release of hormones such as glucagon and cortisol, in response to inadequate glucose transport into the cells; this leads to gluconeogenesis and glycogenolysis, resulting in severe hyperglycemia leading to hyperosmolality and osmotic diuresis
47
Q

The causes of diabetic ketoacidosis

A
  • intentional and unintentional missed or reduced doses of insulin
  • inadequate insulin due to increased insulin needs secondary to stress or infection
  • new onset of type 1 diabetes
48
Q

Clinical Manifestations of Diabetic Ketoacidosis

A

one of polyuria, polydipsia, and polyphagia

  • dehydrated and an electrolyte imbalance such as hyperkalemia or hypokalemia
  • increased serum osmolality also results in a shift of fluid from the intracellular to the extracellular space, causing dilutional hyponatremia (low sodium)
  • at risk for hypovolemia secondary to osmotic diuresis
49
Q

Without treatment of Diabetic Ketoacidosis what happens?

A
  • becomes hypotensive and tachycardic because of the volume loss
  • Kussmaul’s respirations: rapid, deep respirations that occur as a compensatory mechanism for the acidosis
  • fruity, acetone smell to the breath because of the ketone bodies
  • may complain of nausea and vomiting
  • lethargy and coma
50
Q

Diagnosis of DKA

A
  • blood glucose level greater than 250 mg/dL
  • ketonuria (ketones in the urine)
  • Arterial pH of less than or equal to 7.3
  • serum bicarbonate level of less than or equal to 18 mEq/L
  • positive anion gap
51
Q

Treatment of Diabetic Ketoacidosis (DKA)

A
  • fluid replacement with isotonic normal saline
  • correction of electrolyte imbalances, focusing on monitoring and correction of decreased potassium level if necessary, prior to insulin administration
  • insulin administration, usually intravenous delivery to correct the hyperglycemia
52
Q

Why do we use isotonic normal saline for a treatment of DKA?

A

fluid replacement with isotonic normal saline is essential to reverse the dehydration that resulted from the osmotic diuresis

53
Q

Why do we monitor and correct electrolyte imbalances especially potassium in the treatment for DKA?

A

monitoring and correcting electrolyte imbalances is essential to avoid the dysrythmias or neurological complications that can occur with potassium and sodium imbalances
>hyperkalemia may be present because of the movement of positively charged potassium ions out of the cell in effort to maintain homeostasis as positively charged hydrogen ions move into the cell as they accumulate in the extracellular fluid; hypokalemia then ensues as a result of the loss of extracellular potassium in the urine because of the osmotic diuresis; this results in severe total body loss of potassium, making the patient susceptible to lethal arrhythmias
-care must be taken to monitor potassium levels prior to treating the hyperglycemia with insulin; as insulin is administered to decrease the hyperglycemia, potassium will also move back into the cell, worsening hypokalemia. If hypokalemia is present, potassium replacement is a priority

54
Q

Complications of Type 1 diabetes: Hypoglycemia

A
  • can present as acute or life-threatening due to the potentially devastating effects it has on the central nervous system; the central nervous system relies solely on glucose for its energy needs; it needs a constant supply to maintain metabolic functioning and avoid cell death
  • blood glucose level less than 65 mg/dL
55
Q

When does hypoglycemia result?

A

when there is more circulating insulin than is needed to handle the amount of circulating glucose; surplus insulin can be the result of an overly high dose of insulin administered, overly high dose of the oral agents that stimulate insulin release, or reduced clearance of insulin from the body because of renal insufficiency

56
Q

When are patients at risk for hypoglycemia?

A
  • when they have decreased nutritional intake or increased metabolism of glucose through increased exercise
  • alcohol can also reduce blood glucose levels by blunting the release of glucose from the liver; hypoglycemia is more severe when the early signs of low blood glucose are blunted, as in older adults or those who have a change in mental status
57
Q

When blood glucose levels drop below normal levels, the body attempts to raise glucose through the stimulation of the sympathetic nervous system and the release of hormones such as epinephrine, norepinephrine, and glucagon. Symptoms include:

A
  • anxiety
  • hunger
  • palpitations
  • circumoral paresthesia (numbness around lips)
  • sweating
  • shakiness
  • irritability
58
Q

If blood glucose levels continue to drop, reaching levels where the central nervous system is inadequately supplied with glucose, symptoms include:

A
  • difficulty thinking
  • dizziness
  • fatigue
  • sleepiness
  • slurred speech
  • weakness/ lack of coordination
59
Q

If untreated and hypoglycemia progresses further, symptoms can progress to?

A
  • seizures

- coma

60
Q

How to treat hypoglycemia

A

primary management technique consists of the administration of glucose to raise serum glucose levels

  • oral glucose (15-20 g) administration is the preferred treatment for the conscious individual
  • any form of rapidly absorbed carbohydrate may be used; juice, soda, honey, jelly, bread, or crackers
  • after ingestion of carbohydrate blood glucose level should be measured within 15 minutes; if blood glucose levels still reflect hypoglycemia, the treatment should be repeated; once at a normal level the patient should consume a meal or snack to prevent recurrence
61
Q

What if the patient with hypoglycemia is unable to swallow or is unable to swallow and has no IV access?

A
  • if unable to swallow or absorb oral carbohydrates, IV dextrose, 25 to 50 mL of 50% dextrose solution (D50), should be administered
  • If there is no IV access and the patient is unable to swallow or absorb oral carbohydrates, 1 mg of intramuscular glucagon injected should be administered; glucagon mobilizes glucose release from stores in the liver
62
Q

What is a side affect of glucagon when administering it as an injection?

A

nausea and vomiting

-turn patient on their side to avoid aspiration

63
Q

Complications of DM: Dawn Phenomenon

A

the increased blood glucose levels of the dawn phenomenon result from the naturally occurring release of hormones, such as glucagon, cortisol, and growth hormone, in the early morning
-because the body does not have sufficient insulin to control this glucose surge, blood glucose levels rise; this is most likely reflected in higher fasting blood glucose levels in the morning

64
Q

Complications of DM: Somogyi effect

A

much less common than the dawn phenomenon

  • results in increased blood glucose levels due to an excessive insulin dosage at night
  • can occur in a patient who experiences unrecognized low glucose during the night while sleeping; in that circumstance, blood glucose levels drop, and the body responds in the same way as in the dawn phenomenon, releasing growth hormone, cortisol, and catecholamines in an effort to increase blood glucose by releasing glucose stores from the liver; results in a higher than normal glucose levels in the morning
65
Q

How to Determine what is causing the increased blood glucose levels in the early morning: Dawn phenomenon or Somogyi effect

A

the patient needs to check blood glucose levels in the early morning hours, 2 or 3 a.m. for several nights

  • if the blood glucose level is low at 2 or 3 a.m., the high glucose level later in the early morning is due to Somogyi effect
  • if the blood glucose level is high or normal in the early morning, the increased levels later in the morning are due to the dawn phenomenon
66
Q

The clinical manifestations of Type 1 DM are due to what?

A

the hyperglycemia that results from a lack of insulin secreted by the pancreas

  • patients present with polyuria and polydipsia, as well as a hemoconcentration (decreased in plasma volume) in the blood secondary to the increased glucose in the urine, or glucosuria
  • both situations create osmotic shifts in fluid, either from the intracellular space to the vascular space or from the renal tubules into the urine; the resultant volume loss triggers the thirst center in the brain, creating polydipsia
  • excessive hunger and fatigue are due to the inability to utilize glucose for cellular metabolism, resulting in the breakdown of fats and proteins
67
Q

Nursing Diagnoses for Type 1 DM

A
  • Impaired tissue perfusion r/t decreased cardiac output secondary to osmotic diuresis
  • Risk for neurological impairment r/t hypoglycemia
68
Q

Nursing Interventions: Assessment

A

Assess:

  • Vital Signs
  • Serum glucose
  • Potassium levels
  • Intake and Output
  • Carbohydrate Intake at Meals
69
Q

Assessment: Vital Signs

A

decreased blood pressure and increased heart rate are secondary to the fluid volume deficit created by the osmotic diuresis r/t hyperglycemia
-increased respiratory rate, Kussmaul’s breathing, or hyperventilation with fruity breath odor may be evident in DKA in an effort to compensate for the metabolic acidosis

70
Q

Assessment: Serum Glucose

A

increased glucose levels are due to the lack of secretion of insulin from the pancreas
-in a patient already diagnosed with and being treated for type 1 DM, increased glucose levels indicate:
>inadequate or lack of insulin administration
>increased insulin requirements due to stress, such as infection, causing the adrenal release of catecholamines, increasing the hepatic production of glucose
-decreased glucose levels caused by inappropriate insulin administration, such as too much insulin or insulin given while the patient has an inadequate PO intake, can lead to lethargy and coma or death; the brain only uses glucose for cellular metabolism, so it is severely affected by decreased glucose levels

71
Q

Nursing Actions

A
  • Bedside glucose monitoring (finger sticks) done before meal and at bedtime; done to measure the adequacy of glucose control
  • administer insulin as ordered; basal, pre-prandial, or correctional
  • administration of isotonic IV fluids as ordered
72
Q

Actions: administer insulin as ordered; basal, pre-prandial, or correctional

A

administering rapid-acting insulin before meals, preparing for ingestion of carbohydrates, and correcting for random high glucose levels as determined by self-monitoring of blood glucose prior to the meal, in combination with longer-acting insulin once a day, will mimic the action of a healthy pancreas, helping to maintain tight glycemic control
-in patients with questionable or minimal oral intake, prandial and correctional insulins may be administered together after meals after adequate carbohydrate intake has been confirmed

73
Q

Actions: administration of isotonic IV fluids as ordered

A

IV fluids may be necessary to replace the volume lost as a result of osmotic diuresis

74
Q

Nursing Teaching

A
  • signs of hypo and hyperglycemia
  • subcutaneous insulin administration
  • common sites
  • SubQ technique
  • syringe size
  • rotating sites
  • infection control
  • medication education
  • regular blood glucose monitoring
  • healthy lifestyle that includes diet and exercise
75
Q

Teaching: Common sites of SubQ injection

A

common sites that provide good absorption (starting with the area of best absorption) include the abdomen, upper arm, thigh, and buttocks

76
Q

Teaching: SubQ injection technique

A

to ensure injection into the subcutaneous tissue, pinch the skin at the injection site and insert the needle straight in at a 90-degree angle
-if the patient is very thin with very small amounts of subcutaneous tissue, the needle should be inserted at a 45-degree angle

77
Q

Teaching: SubQ syringe size for insulin

A

choose the syringe size (1 mL, 0.5 mL, 0.3 mL) that best matches your insulin dose

  • the smaller syringes allow for more accurate measurement of smaller insulin dosages
  • if available, an insulin pen can be used and instructions given to the patient on accurate use and storage
78
Q

Teaching: Rotating sites

A

insulin is administered subcutaneously

  • it is a protein substance
  • if taken orally it is broken down in the GI tract, rendering it useless
  • rotating sites helps decrease lipohypertrophy (fat deposits in the skin) or lipoatrophy (loss of fatty tissue)
  • rotating sites within one area rather than moving from area to area helps decrease absorption variability from day to day; this can be done by injecting a new shot at least an inch away from the last injection site
79
Q

Lipohypertrophy

A

fat deposits in the skin

-can develop if you do not rotate sites

80
Q

Lipoatrophy

A

loss of fatty tissue

-can develop if you do not rotate sites

81
Q

Teaching: Infection Control

A

immediately discard used syringes and needles; use a new needle for each dose

82
Q

Teaching: Medication Education

A

lifelong insulin administration is required for cellular metabolism
-increased stress, infection, activity level, increased ingestion of carbohydrates, and decreased PO intake all alter insulin requirements

83
Q

Teaching: Regular blood glucose monitoring

A

via finger stick or alternate site testing if appropriate

  • regular checks help determine the adequacy of insulin dosage and maintain glycemic targets
  • continuous glucose monitoring may be an option for the patient requiring more glucose information or to reduce the number of finger sticks
84
Q

Evaluating Care Outcomes

A

the patient with type 1 DM can lead a long and healthy life with strict adherence to the treatment regimen and good self-management skills

  • the tight glycemic control necessary to avoid the complications associated with DM is best achieved through active monitoring of blood glucose levels and treatment with insulin as indicated
  • nutrition, patient education, self-management, and detection and prevention of complications are essential components of successful daily management of DM

Nursing 172 (120 decks)

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