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
2
Q
Cause of diabetes mellitus?
A
Genetic, autoimmune, and environmental disorders
3
Q
Normal blood glucose range:
A
70-120 mg/dL
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)
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
6
Q
Bolus Insulin
A
Released when food is metabolized; (short acting); used at mealtimes to combat postprandial hyperglycemia and also used at bedtime
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
8
Q
Role of insulin in the metabolism of glucose
A
Stimulates storage of glucose as glycogen in liver and muscle; inhibits gluconeogenesis
9
Q
Role of insulin in the metabolism of fat
A
enhances fat deposition of adipose tissue
10
Q
Role of insulin in the metabolism of protein
A
^ protein synthesis
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)
12
Q
Causes of metabolic syndrome
A
- obesity
- sedentary lifestyle
- urbanization
- certain ethnicities
13
Q
Treatment of metabolic syndrome
A
Change of lifestyle
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)
15
Q
Fasting plasma glucose level (FPG)
A
level >126; No caloric intake for at least 8 hours
16
Q
Random plasma glucose
A
level >200; For patients with classic symptoms of hyperglycemia
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
18
Q
Glycosylated hemoglobin test (HbA1C)
A
Keep level below 7.0%; useful in evaluating long-term glycemic levels
19
Q
What was the former name of type 1 diabetes?
A
Juvenile-onset diabetes; Insulin dependent diabetes
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
21
Q
Of all types of diabetes, what is the prevalence of type 1 diabetes?
A
5-10% of all types
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
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
24
Q
Nutritional status of someone who presents type 1 diabetes
A
Thin, normal, or obese
25
Common symptoms of type 1 diabetes
polydipsia (thirst), polyuria, polyphagia (hunger), fatigue, weight loss; caused by hyperglycemia and the accompanying spillover of excess glucose in the urine
26
Is exogenous insulin required for type 1?
Yes; Without insulin the patient will develop DKA, a life-threatening condition resulting in metabolic acidosis
27
Why ketosis results if insulin in type 1 is omitted
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
28
What was the former name of type 2 diabetes?
Adult-onset diabetes; Non-insulin dependent
29
What is the typical age of onset for type 2 diabetes?
Usually 35 years or older but can occur at any age
30
Of all types of diabetes, what is the prevalence of type 2 diabetes?
over 90% of all types
31
What is the etiology and pathophysiology of type 2 diabetes?
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
32
Describe the onset of type 2 diabetes
Insidious- may go undiagnosed for years
33
Nutritional status of someone who presents type 2 diabetes
Obese or Normal
34
Common symptoms of type 2 diabetes
Frequently none, fatigue, recurrent infections, recurrent vaginal yeast or monilia infections, prolonged wound healing, and visual changes
35
Is exogenous insulin required for type 2?
Required for some
36
Why ketosis results if insulin in type 2 is omitted
refer to answer for type 1, not seen much in type two diabetes
37
What is HbA1C?
indicates the amount of glucose that has been attached to hemoglobin molecules over their lifespan (determines glycemic levels over time also)
38
Relationship between HbA1C and Blood glucose
HbA1C shows what your blood glucose is on average for past 90-120 days.
39
Goals of HbA1C
<7.0%; v risk of retinopathy, nephropathy, &neuropathy
40
Post Prandial Blood Glucose Level
<180 mg/dL; glucose after a meal
41
Gestational Diabetes
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
42
Overall nutritional goals for PWD
Assist people with diabetes in making healthy nutritional choices, eating a varied diet, and maintain exercise habits that will lead to metabolic control
43
Type 1 meal planning
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
44
Type 2 meal planning
Based on achieving glucose, lipid, and blood pressure goals
45
Carbohydrate counting
used to keep track of the amount of carbs they eat with each meal per day
46
Insulin-carb ratio
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
47
Benefits of exercise
^ 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
48
Risks of exercise
Hypoglycemia, stress which increases counterirregulatory hormones (^ glucose)
49
When should a person test the blood glucose?
Most often before meals; before and after exercise, when hypoglycemia is suspected
50
Oral Agents
Work on three defects of type 2:
1. Insulin resistance
2. v insulin production
3. ^ hepatic glucose production
51
Sulfonylureas (Glipizide, glyburide, glimepiride)
^ 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
Biguanides (Metformin)
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
Thiazolidinediones (proglitazone, rosiglitazone)
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
Alpha-Glucodidase Inhibitors (Acarbose, miglitol)
Slows down the absorption of carbohydrate in the small intestine.
*Side effects: gas, abdominal pain, diarrhea
55
Losartan
Angiotensin II receptor antagonist- Helps lower BP, found to delay occurrence of nephropathy in PWD,
56
Endogenous Insulin
Self-made insulin
57
Exogenous Insulin
Injected insulin
58
Insulin Administration
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
Insulin Rate of Absorption
Fastest absorption is in the abdomen, then the thigh and arm
60
Insulin Pump
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
Rapid-acting Insulin
Novolog;
- Bolus
- Clear
- Onset: 15 min
- Peak: 60-90 min
- Duration: 3-4 hours
62
Short-Acting Insulin
Regular;
- Bolus
- Clear
- Onset: 30 min-1 hour
- Peak: 2-3 hours
- Duration: 3-6 hours
63
Intermediate Acting Insulin
NPH;
- Basal
- Cloudy
- Onset: 2-4 hours
- Peak: 4-10 hours
- Duration: 10-16 hours
64
Long-Acting Insulin
Lantus;
- Basal
- Clear
- Onset: 1-2 hours
- Peak: no peak
- Duration: 24+ hours
65
Insulin Regimens: Single Dose/Day
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
Insulin Regimens: Split-Mix
NPH AND regular OR rapid; BID: before breakfast and at dinner
*PT. must adhere to set meal plan
67
Insulin Regimens: Three shot regimen
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
Insulin Regimens: Basal-bolus
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
Lypodystrophy
(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
The Somogyi Effect
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
Dawn Phenomenon
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
What is Hypoglycemia?
Low blood glucose levels (<70 mg/dL)
| -too much insulin in proportion to available glucose in blood
73
Causes of Hypoglycemia
- 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
Hypoglycemic unawareness
-person doesn't experience warning signs or symptoms of hypoglycemia until glucose levels reach critical point
75
Symptoms of Hypoglycemia
- 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
Treatment of Hypoglycemia
ingesting 15-20 g of simple carbs (fruit juice, soda, etc)
77
Rule of 15
Treat hypoglycemia with 15 g of carbs then check blood glucose in 15 min. (repeat as needed)
78
When can someone experience symptoms of hypoglycemia without having a blood glucose that meets the criteria of hypoglycemia?
When a high level of glucose falls rapidly
79
What is Diabetic Ketoacidosis? (DKA)
life-threatening condition caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration
80
Who is more likely to get DKA?
Type 1 diabetes because their pancreas can't produce insulin naturally
81
What are the precipitating factors of DKA?
- illness and infection
- inadequate insulin dosage
- undiagnosed type 1 diabetes
- poor self management
- neglect
82
What is Ketosis?
Alters pH balance, causing metabolic acidosis to occur
83
Why does Ketosis occur?
- 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
What impact does Ketosis have on fluid and electrolyte imbalance?
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
Symptoms of DKA
- Poor skin turgor
- dry mucous membranes
- tachycardia
- orthostatic hypotension
86
What is the priority, initial treatment of DKA
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
When and why would a pt. with DKA be given IV fluid containing glucose?
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
Hyperosmolar hyperglycemic syndrome (HHS)
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
Who is more likely to get HHS? Type 1 or Type 2?
Type 2 because they are insulin producing which prevent DKA; type 1 would go straight to DKA
90
Precipitating factors of HHS
- Infections of the urinary tract
- pneumonia
- sepsis
- any acute illness
- and newly diagnosed type 2 diabetes
91
Why do blood glucoses reach higher levels in HHS when compared to DKA?
b/c pt. usually has enough circulating insulin and does not cause ketoacidosis; leads to having fewer symptoms and glucose climbs
92
Why would HHS initially be confused with the onset of a stroke?
b/c high blood glucose levels ^ serum osmolality and produce more severe neurologic manifestations such as somnolence, coma, seizures, hemiparesis, and aphasia
93
What is the priority, initial treatment of HHS
Immediate IV administration
94
What is angiopathy?
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
Theories regarding how poorly controlled diabetes causes cell and tissue damage
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
Macrovascular Angiopathy
Diseases of the large and medium sized blood vessels that occur with greater frequency and with an earlier onset in people with diabetes
97
What systems of the body are affected by Macrovascular Angiopathy?
Cerebrovascular, Cardiovascular, and Peripheral vascular
98
Modifiable factors that can decrease the risk of cardiovascular disease in PWD?
- obesity
- smoking
- hypertension
- high fat intake
- sedentary lifestyle
99
Level of BP for PWD
BP- 130/80
100
Level of LDL's for PWD
LDL Cholesterol- <100 mg/dL
101
Level of Triglycerides for PWD
Triglycerides- <150 mg/dL
102
Level of HDL's for PWD
>50 mg/dL
103
Microvascular Angiopathy
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
Diabetic Retinopathy
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
Treatment of Diabetic Retinopathy
Earliest and most treatable stages produce no vision changes, PWD should have an annual dilated eye exam
106
Non-proliferative Retinopathy
partial occlusion of small blood vessel in the retina causes microaneurysms (vessel swelling) to develop in capillary walls
107
Proliferative Retinopathy
Produces new blood vessels in retina because of occlusion and are very weak (very severe)
108
Surgical procedures of retinopathy
- Laser photocoagulation therapy
| - Virectomy (advanced proliferative retinopathy)
109
Diabetic Nephropathy
microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney
110
What is the impact of nephropathy?
Leading cause of end stage renal disease
111
How often should a PWD be screened for nephropathy?
Annually; measurement of the albumin to creatinine ration in a random spot urine collection
112
How can nephropathy be avoided?
have a near-normal blood glucose achieved and maintained
113
If diagnosed with nephropathy, what drugs delay or prevent nephropathy?
Ace inhibitors drugs or angiotensin II (treat hypertension or delay progression of nephropathy
114
Diabetic Neuropathy
nerve damage that occurs because of the metabolic derangements associated with diabetes.
Two catergories:
1. Sensory neuropathy
2. Autonomic neruopathy
115
Etiology of Neuropathy
-persistant hyperglycemia leads to an accumulation of Sorbitol and fructose in nerves that causes damage by unknown mechanism
116
What is sensory neuropathy and what are the signs and symptoms?
Effects peripheral nervous system;
- loss of sensation
- abnormal sensations
- pain
- paresthesias (tingling, burning)
117
What medications are used to treat sensory neuropathy?
Topical creams (capsaicin: Zostrix), tricyclic antidepressants (amitriptyline), selective serotonin and norepinephrine reuptake inhibitors (duloxetine), and antiseizure (gabapentin)
118
Common form of sensory neuropathy
Distal symmetric neuropathy, which affects the hands and/or feet bilaterally. Sometimes referred to as stocking-glove neuropathy
119
Autonomic Neuropathy
Damage to nerves that control HR, digestion, and motor function
120
Body systems that are affected by Autonomic Neuropathy
Can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention
121
How do microvascular and macrovascular complications of diabetes both play a role in foot disease??????
Could lead to amputation; combination of microvascular and macrovascular diseases place the pt. at risk for injury
122
How is Loss of protective sensation (LOPS) tested for?
Monofilament- thin flexible filament to several spots on the planter surface and ask if it is felt.
123
Pancreas transplantation
- 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
PWD Mental Illnesses
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.
