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Exam 3 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is diabetes mellitus?

A

A chronic multisystem disorder of glucose metabolism related to absent or insufficient insulin supplies, impaired utilization of insulin, or both

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2
Q

Cause of diabetes mellitus?

A

Genetic, autoimmune, and environmental disorders

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3
Q

Normal blood glucose range:

A

70-120 mg/dL

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4
Q

Pre-diabetes

A

a condition in which blood glucose levels are higher than normal but not high enough for a diagnoses of diabetes; usually will develop type 2 diabetes within 10 years if no preventative measures are taken

Fasting BG: 100-126
(may already have long term damage in heart and blood vessels)

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5
Q

Basal Insulin

A

Continuously released into bloodstream in small increments; (long-acting); used to maintain a background level of insulin throughout the day

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6
Q

Bolus Insulin

A

Released when food is metabolized; (short acting); used at mealtimes to combat postprandial hyperglycemia and also used at bedtime

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7
Q

Counterregulatory Hormones

A

Glucagon, epinephrine, growth hormone, cortisol; Oppose the effects of insulin.

  • ^ blood glucose levels by stimulating glucose production and output by the liver
  • v movement of glucose into cells
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8
Q

Role of insulin in the metabolism of glucose

A

Stimulates storage of glucose as glycogen in liver and muscle; inhibits gluconeogenesis

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9
Q

Role of insulin in the metabolism of fat

A

enhances fat deposition of adipose tissue

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10
Q

Role of insulin in the metabolism of protein

A

^ protein synthesis

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11
Q

What is metabolic syndrome?

A

Cluster of abnormalities that act synergistically to greatly ^ risk for CV disease and diabetes (High bp, high blood sugar, unhealthy cholesterol levels, etc)

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12
Q

Causes of metabolic syndrome

A
  • obesity
  • sedentary lifestyle
  • urbanization
  • certain ethnicities
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13
Q

Treatment of metabolic syndrome

A

Change of lifestyle

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14
Q

Four methods to diagnose diabetes

A

Fasting plasma glucose level, random plasma glucose measurement, two hour oral glucose tolerance test, glycosylated hemoglobin test (HbA1C)

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15
Q

Fasting plasma glucose level (FPG)

A

level >126; No caloric intake for at least 8 hours

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16
Q

Random plasma glucose

A

level >200; For patients with classic symptoms of hyperglycemia

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17
Q

2-hour plasma glucose level (Oral glucose tolerance test)

A

level >200; OGTT; using a glucose load of 75g. Can be inaccurate by severe restrictions of dietary carbs, acute illness, medications, and bed rest

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18
Q

Glycosylated hemoglobin test (HbA1C)

A

Keep level below 7.0%; useful in evaluating long-term glycemic levels

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19
Q

What was the former name of type 1 diabetes?

A

Juvenile-onset diabetes; Insulin dependent diabetes

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20
Q

What is the typical age of onset for type 1 diabetes?

A

Most often occurs in people who are under 30 years of age, with a peak onset between ages 11 and 13, but can occur at any age

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21
Q

Of all types of diabetes, what is the prevalence of type 1 diabetes?

A

5-10% of all types

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22
Q

What is the etiology and pathophysiology of type 1 diabetes?

A

Type 1 is the end result of a long-standing process where the body’s own t-cells attack and destroy pancreatic B cells, which are the source of the body’s insulin

*Auto antibodies to the islet cells cause a reduction of 80-90% of normal B-cell function before hyperglycemia and other manifestations occur

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23
Q

Describe the onset of type 1 diabetes

A

Initial manifestations are usually acute because the onset is rapid, although disease may be present for years

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24
Q

Nutritional status of someone who presents type 1 diabetes

A

Thin, normal, or obese

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25
Q

Common symptoms of type 1 diabetes

A

polydipsia (thirst), polyuria, polyphagia (hunger), fatigue, weight loss; caused by hyperglycemia and the accompanying spillover of excess glucose in the urine

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26
Q

Is exogenous insulin required for type 1?

A

Yes; Without insulin the patient will develop DKA, a life-threatening condition resulting in metabolic acidosis

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27
Q

Why ketosis results if insulin in type 1 is omitted

A

Glucose can’t be properly used for energy so the body breaks down fat stores as a secondary source of fuel. Ketones are bi-products of fat metabolism that cause serious problems when excessive in the blood.
*Ketosis alters pH balance

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28
Q

What was the former name of type 2 diabetes?

A

Adult-onset diabetes; Non-insulin dependent

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29
Q

What is the typical age of onset for type 2 diabetes?

A

Usually 35 years or older but can occur at any age

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30
Q

Of all types of diabetes, what is the prevalence of type 2 diabetes?

A

over 90% of all types

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31
Q

What is the etiology and pathophysiology of type 2 diabetes?

A

The pancreas usually continues to produce some endogenous (self-made) insulin. However, the insulin that is produced is either insufficient for the needs of the body and/or is poorly used by the tissues

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32
Q

Describe the onset of type 2 diabetes

A

Insidious- may go undiagnosed for years

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33
Q

Nutritional status of someone who presents type 2 diabetes

A

Obese or Normal

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34
Q

Common symptoms of type 2 diabetes

A

Frequently none, fatigue, recurrent infections, recurrent vaginal yeast or monilia infections, prolonged wound healing, and visual changes

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35
Q

Is exogenous insulin required for type 2?

A

Required for some

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36
Q

Why ketosis results if insulin in type 2 is omitted

A

refer to answer for type 1, not seen much in type two diabetes

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37
Q

What is HbA1C?

A

indicates the amount of glucose that has been attached to hemoglobin molecules over their lifespan (determines glycemic levels over time also)

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38
Q

Relationship between HbA1C and Blood glucose

A

HbA1C shows what your blood glucose is on average for past 90-120 days.

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39
Q

Goals of HbA1C

A

<7.0%; v risk of retinopathy, nephropathy, &neuropathy

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40
Q

Post Prandial Blood Glucose Level

A

<180 mg/dL; glucose after a meal

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41
Q

Gestational Diabetes

A

develops during pregnancy and is detected at 24-48 weeks of gestation (usually by an oral glucose tolerance test)
*Risk for developing type 2 diabetes in 5-10 years is increased

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42
Q

Overall nutritional goals for PWD

A

Assist people with diabetes in making healthy nutritional choices, eating a varied diet, and maintain exercise habits that will lead to metabolic control

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43
Q

Type 1 meal planning

A

day-to-day consistency in timing and amount of food eaten is important for those individuals using conventional, fixed insulin regimens; Pt using rapid acting insulin can make adjustments in dosage before the meal based on the current blood glucose level and the carbohydrate content of the meal

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44
Q

Type 2 meal planning

A

Based on achieving glucose, lipid, and blood pressure goals

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45
Q

Carbohydrate counting

A

used to keep track of the amount of carbs they eat with each meal per day

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46
Q

Insulin-carb ratio

A

of grams of carbs covered by each unit of rapid or short-acting insulin; 1 unit of insulin = 15 g of carbs (ratio can vary depending on person

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47
Q

Benefits of exercise

A

^ insulin receptor sites in the tissue and can have a direct effect on lowering blood glucose levels, contributes to weight loss, v need for diabetic medicines, v triglyceride and LDL cholesterol levels, ^HDL, vBP, & improve circulation

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48
Q

Risks of exercise

A

Hypoglycemia, stress which increases counterirregulatory hormones (^ glucose)

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49
Q

When should a person test the blood glucose?

A

Most often before meals; before and after exercise, when hypoglycemia is suspected

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50
Q

Oral Agents

A

Work on three defects of type 2:

  1. Insulin resistance
  2. v insulin production
  3. ^ hepatic glucose production
51
Q

Sulfonylureas (Glipizide, glyburide, glimepiride)

A

^ insulin production from the pancreas by sensitizing the pancreatic B cells.

  • Can cause hypoglycemia, photosensitivity, and weight gain
  • Often added to the treatment regimen if metformin and lifestyle interventions are not effective
  • Type 1 should not take this
52
Q

Biguanides (Metformin)

A

Biguanide glucose lowering agent. Primary action is to reduce glucose production by the liver;

  • Side effects: Diarrhea, sore muscles from lactic acidosis
  • helps your cells (particularly muscles) to take in sugar from the bloodstream
  • Also decreases the amount of sugar absorbed by the body from the foods you eat
53
Q

Thiazolidinediones (proglitazone, rosiglitazone)

A

Most effective for people who have insulin resistance; Improve insulin sensitivity, transport, and utilization of tissues

  • Side effects are: weight gain, edema, ^ risk for CV, MI, or stroke
  • *Risk for hypoglycemia when used with sulfonylureas or insulin
  • Type 1 and DKA should not take this
54
Q

Alpha-Glucodidase Inhibitors (Acarbose, miglitol)

A

Slows down the absorption of carbohydrate in the small intestine.
*Side effects: gas, abdominal pain, diarrhea

55
Q

Losartan

A

Angiotensin II receptor antagonist- Helps lower BP, found to delay occurrence of nephropathy in PWD,

56
Q

Endogenous Insulin

A

Self-made insulin

57
Q

Exogenous Insulin

A

Injected insulin

58
Q

Insulin Administration

A

Routine administration of insulin is most commonly done by means of subcutaneous injection, intravenous administration of regular insulin can be done when immediate onset of action is desired

59
Q

Insulin Rate of Absorption

A

Fastest absorption is in the abdomen, then the thigh and arm

60
Q

Insulin Pump

A

Continuous subcutaneous insulin infusion that is programmed to deliver a continuous infusion of short-acting insulin 24 hours a day with boluses at mealtime

61
Q

Rapid-acting Insulin

A

Novolog;

  • Bolus
  • Clear
  • Onset: 15 min
  • Peak: 60-90 min
  • Duration: 3-4 hours
62
Q

Short-Acting Insulin

A

Regular;

  • Bolus
  • Clear
  • Onset: 30 min-1 hour
  • Peak: 2-3 hours
  • Duration: 3-6 hours
63
Q

Intermediate Acting Insulin

A

NPH;

  • Basal
  • Cloudy
  • Onset: 2-4 hours
  • Peak: 4-10 hours
  • Duration: 10-16 hours
64
Q

Long-Acting Insulin

A

Lantus;

  • Basal
  • Clear
  • Onset: 1-2 hours
  • Peak: no peak
  • Duration: 24+ hours
65
Q

Insulin Regimens: Single Dose/Day

A

A. Intermediate (NPH) at bedtime (provide nighttime coverage)
OR
B. Long-acting in the AM or bedtime (24 hours with no peaks (v chance of hypoglycemia) )

66
Q

Insulin Regimens: Split-Mix

A

NPH AND regular OR rapid; BID: before breakfast and at dinner
*PT. must adhere to set meal plan

67
Q

Insulin Regimens: Three shot regimen

A
  1. NPH AND regular OR rapid before breakfast; 2. and regular or rapid before dinner; 3. NPH at bedtime
    * Potential is reduced for 2-3 AM hypoglycemia
68
Q

Insulin Regimens: Basal-bolus

A
  1. Regular OR rapid before breakfast, lunch, and dinner; AND long-acting once a day
  2. Regular OR rapid before breakfast, lunch, and dinner; AND NPH twice a day

*Good for postprandial control; flexibility at mealtimes

69
Q

Lypodystrophy

A

(atrophy of subcutaneous tissue) may occur if the same injection sites are used frequently. Incidence as decreased with the use of human insulin

  • recommended to rotate within the same site
  • lumps and dents from repeated injection
70
Q

The Somogyi Effect

A

rebound effect in which an overdose of insulin induces hypoglycemia. Usually occurring during the hours of sleep, the Somogyi effect produces a decline in blood glucose levels in response to too much insulin

  • Wake up with hyperglycemia bc hormones are released to correct during the night
  • Treatment: insulin dose affecting early morning blood glucose is v
71
Q

Dawn Phenomenon

A

Hyperglycemia that is present on awakening in the morning resulting from the release of counterregulatory hormones in the pre-dawn hours
*Treatment: adjust timing of insulin administration or ^ in insulin

72
Q

What is Hypoglycemia?

A

Low blood glucose levels (<70 mg/dL)

-too much insulin in proportion to available glucose in blood

73
Q

Causes of Hypoglycemia

A
  • Mismatch in the timing of food intake and the peak action of insulin or oral hypoglycemic agents that increase endogenous insulin secretion
  • Unusual amount of exercise
74
Q

Hypoglycemic unawareness

A

-person doesn’t experience warning signs or symptoms of hypoglycemia until glucose levels reach critical point

75
Q

Symptoms of Hypoglycemia

A
  • Glucose <70 mg/dL
  • Cold, clammy skin
  • rapid heartbeat
  • headache
  • numbness of finger, toes, and mouth
  • headache
  • nervousness
  • tremors
  • faintness
  • hunger
  • changes in vision
76
Q

Treatment of Hypoglycemia

A

ingesting 15-20 g of simple carbs (fruit juice, soda, etc)

77
Q

Rule of 15

A

Treat hypoglycemia with 15 g of carbs then check blood glucose in 15 min. (repeat as needed)

78
Q

When can someone experience symptoms of hypoglycemia without having a blood glucose that meets the criteria of hypoglycemia?

A

When a high level of glucose falls rapidly

79
Q

What is Diabetic Ketoacidosis? (DKA)

A

life-threatening condition caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration

80
Q

Who is more likely to get DKA?

A

Type 1 diabetes because their pancreas can’t produce insulin naturally

81
Q

What are the precipitating factors of DKA?

A
  • illness and infection
  • inadequate insulin dosage
  • undiagnosed type 1 diabetes
  • poor self management
  • neglect
82
Q

What is Ketosis?

A

Alters pH balance, causing metabolic acidosis to occur

83
Q

Why does Ketosis occur?

A
  • Insulin is insufficient and glucose cannot be properly used for energy so body breaks down fat stores for fuel.
  • The bi-products of fat metabolism is ketones and they can cause problems if excessive in the blood
84
Q

What impact does Ketosis have on fluid and electrolyte imbalance?

A

Low insulin causes the glucose not to be used properly and glucose ^, adding to osmotic diuresis.
-If untreated, there is severe depletion of Na, K, Cl, Mg, PO43; vomiting also occurs

85
Q

Symptoms of DKA

A
  • Poor skin turgor
  • dry mucous membranes
  • tachycardia
  • orthostatic hypotension
86
Q

What is the priority, initial treatment of DKA

A

Ensure pt. airway and establish IV access and begin fluid and electrolyte replacement (raise BP and provide urinary system with sufficient fluids to correct ketoacidic problems)

87
Q

When and why would a pt. with DKA be given IV fluid containing glucose?

A

When blood glucose levels approach 250 mg/dL (can cause complications if it falls too quickly- ex: cerebral edema)
-36-54 mg/dL per hour

88
Q

Hyperosmolar hyperglycemic syndrome (HHS)

A

life-threatening syndrome that can occur in the pt. with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular depletion

89
Q

Who is more likely to get HHS? Type 1 or Type 2?

A

Type 2 because they are insulin producing which prevent DKA; type 1 would go straight to DKA

90
Q

Precipitating factors of HHS

A
  • Infections of the urinary tract
  • pneumonia
  • sepsis
  • any acute illness
  • and newly diagnosed type 2 diabetes
91
Q

Why do blood glucoses reach higher levels in HHS when compared to DKA?

A

b/c pt. usually has enough circulating insulin and does not cause ketoacidosis; leads to having fewer symptoms and glucose climbs

92
Q

Why would HHS initially be confused with the onset of a stroke?

A

b/c high blood glucose levels ^ serum osmolality and produce more severe neurologic manifestations such as somnolence, coma, seizures, hemiparesis, and aphasia

93
Q

What is the priority, initial treatment of HHS

A

Immediate IV administration

94
Q

What is angiopathy?

A

Damage to blood vessels, secondary to chronic hyperglycemia
-Divided into two categories (macrovascular and microvascular)

**one of the leading causes of diabetes related deaths

95
Q

Theories regarding how poorly controlled diabetes causes cell and tissue damage

A
  1. accumulation of damaging by-products of glucose metabolism (damage of nerve cells)
  2. formation of abnormals glucose molecules
  3. Derangement in RBC function that leads to v oxygen to tissue
96
Q

Macrovascular Angiopathy

A

Diseases of the large and medium sized blood vessels that occur with greater frequency and with an earlier onset in people with diabetes

97
Q

What systems of the body are affected by Macrovascular Angiopathy?

A

Cerebrovascular, Cardiovascular, and Peripheral vascular

98
Q

Modifiable factors that can decrease the risk of cardiovascular disease in PWD?

A
  • obesity
  • smoking
  • hypertension
  • high fat intake
  • sedentary lifestyle
99
Q

Level of BP for PWD

A

BP- 130/80

100
Q

Level of LDL’s for PWD

A

LDL Cholesterol- <100 mg/dL

101
Q

Level of Triglycerides for PWD

A

Triglycerides- <150 mg/dL

102
Q

Level of HDL’s for PWD

A

> 50 mg/dL

103
Q

Microvascular Angiopathy

A

Thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia

*Those without diabetes don’t get microvascular angiopathy

**Takes 10-20 years after onset to develop

104
Q

Diabetic Retinopathy

A

process of microvascular damage to the retina as a result of chronic hyperglycemia in pt. with diabetes
Two types: proliferative and non-proliferative

**blindness is the impact

105
Q

Treatment of Diabetic Retinopathy

A

Earliest and most treatable stages produce no vision changes, PWD should have an annual dilated eye exam

106
Q

Non-proliferative Retinopathy

A

partial occlusion of small blood vessel in the retina causes microaneurysms (vessel swelling) to develop in capillary walls

107
Q

Proliferative Retinopathy

A

Produces new blood vessels in retina because of occlusion and are very weak (very severe)

108
Q

Surgical procedures of retinopathy

A
  • Laser photocoagulation therapy

- Virectomy (advanced proliferative retinopathy)

109
Q

Diabetic Nephropathy

A

microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney

110
Q

What is the impact of nephropathy?

A

Leading cause of end stage renal disease

111
Q

How often should a PWD be screened for nephropathy?

A

Annually; measurement of the albumin to creatinine ration in a random spot urine collection

112
Q

How can nephropathy be avoided?

A

have a near-normal blood glucose achieved and maintained

113
Q

If diagnosed with nephropathy, what drugs delay or prevent nephropathy?

A

Ace inhibitors drugs or angiotensin II (treat hypertension or delay progression of nephropathy

114
Q

Diabetic Neuropathy

A

nerve damage that occurs because of the metabolic derangements associated with diabetes.
Two catergories:
1. Sensory neuropathy
2. Autonomic neruopathy

115
Q

Etiology of Neuropathy

A

-persistant hyperglycemia leads to an accumulation of Sorbitol and fructose in nerves that causes damage by unknown mechanism

116
Q

What is sensory neuropathy and what are the signs and symptoms?

A

Effects peripheral nervous system;

  • loss of sensation
  • abnormal sensations
  • pain
  • paresthesias (tingling, burning)
117
Q

What medications are used to treat sensory neuropathy?

A

Topical creams (capsaicin: Zostrix), tricyclic antidepressants (amitriptyline), selective serotonin and norepinephrine reuptake inhibitors (duloxetine), and antiseizure (gabapentin)

118
Q

Common form of sensory neuropathy

A

Distal symmetric neuropathy, which affects the hands and/or feet bilaterally. Sometimes referred to as stocking-glove neuropathy

119
Q

Autonomic Neuropathy

A

Damage to nerves that control HR, digestion, and motor function

120
Q

Body systems that are affected by Autonomic Neuropathy

A

Can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention

121
Q

How do microvascular and macrovascular complications of diabetes both play a role in foot disease??????

A

Could lead to amputation; combination of microvascular and macrovascular diseases place the pt. at risk for injury

122
Q

How is Loss of protective sensation (LOPS) tested for?

A

Monofilament- thin flexible filament to several spots on the planter surface and ask if it is felt.

123
Q

Pancreas transplantation

A
  • used as a treatment option for pt. with type 1 diabetes. Most commonly done for pt. with end stage renal disease and who have had or plan to have a kidney transplant.
  • Pancreas transplants alone are rare
124
Q

PWD Mental Illnesses

A

Pt. needs to be assessed for signs and symptoms of depression at each visit

*women with type 1 diabetes have an ^ risk of developing an eating disorder in comparison to women without diabetes.

Exam 3 (6 decks)

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