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133 Cards in this Set
- Front
- Back
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Type I or Type II Diabetes
known as Insulin-Dependent Diabetes |
Type I –
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Type I or Type II Diabetes
known as non-insulin dependent diabetes |
Type II
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Type I or Type II Diabetes
-beta cell destruction leading to insulin deficiency |
Type I
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Type I or Type II Diabetes
-autoimmune response -idiopathic (we don’t know why) |
Type I
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Type I or Type II Diabetes
-also known as juvenile onset diabetes |
Type I
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Type I or Type II Diabetes
-symptoms: abrupt onset, thirst, weight loss |
Type I
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Type I or Type II Diabetes
-etiology: viral infection |
Type I
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Type I or Type II Diabetes
-pathology: pancreatic beta cell destruction |
Type I
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Type I or Type II Diabetes
Intracellular hypoglycemia- cuz insulin can’t get into the cell so the body goes after the liver…the liver then produces more sugar (glucogenesis) |
Type I
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Type I or Type II Diabetes
If you can’t get the sugar into the cells, this process doesn’t stop. Inside the cells is when the signal gets stopped. |
Type I
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Type I or Type II Diabetes
When the body used up what they have in the liver, it uses fats, ketoacidiosis. |
type 1
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Type I or Type II Diabetes
can get ketoacidosis |
type 1
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Type I or Type II Diabetes
Formally known as : Insulin-Dependent Diabetes (IDDM) |
type 1
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Type I or Type II Diabetes
Often diagnosed under age 30, frequently in childhood |
type 1
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Type I or Type II Diabetes
Seen as an “autoimmune” disease in which “self” takes action against the Beta cells in the pancreas, destroying their insulin-secreting capacity. |
type 1
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Type I or Type II Diabetes
Blood markers: antibodies, (don’t have to know these, just know you can look for antibodies) islet cell antibodies (ICAs) insulin autoantibodies (IAAs) Glutamic acid decarboxylase autoantibodies (GAD) Tyrosine phosphate autoantibodies |
type 1
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Type I or Type II Diabetes
Genetic risk link |
type 1
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Type I or Type II Diabetes
-insulin resistance with insulin deficiency |
2
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Type I or Type II Diabetes
secretory deficit with insulin resistance |
2
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Type I or Type II Diabetes
happens in a pt who is older and obese. Whenever you eat a high carb product it is a stimulus that tells the pancreas to let out some insulin . If you hyperstimulate the beta cells, you will burn it out |
2
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Type I or Type II Diabetes
-also called adult onset diabetes |
2
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Type I or Type II Diabetes
-etiology: not known |
2
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Type I or Type II Diabetes
-pathology: insulin resistance and dysfunctional pancreatic beta cell |
2
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Type I or Type II Diabetes
Formally Known as : Non-Insulin Dependent Diabetes (NIDDM) |
2
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Type I or Type II Diabetes
-Usually occurs in older adults and those that are obese. But this disease can occur at any age. |
2
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Type I or Type II Diabetes
-Begins with insulin resistance, a condition in which fat, muscle, and liver cells do not use insulin properly |
2
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Type I or Type II Diabetes
- At first, the pancreas keeps up with the added demand by producing more insulin. In time, however, it loses the ability to secrete enough insulin in response to meals. There is a huge demand placed on the pancreas. what inhibits the absorption of glucose into the cell. |
2
obesity (adipose tissue) --- Any pt above BMI has a risk, regardless of the age |
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Type I or Type II Diabetes
-There is a reduction in the ability of cells to respond to insulin (resistance), poor control of liver glucose output, & decreased Beta cell function |
2
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Type I or Type II Diabetes
Heredity plays a major role in this Type |
2
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Type I or Type II Diabetes
-Adolescence are the largest growing population who are obese, next group is woman over 35 |
2
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Type I or Type II Diabetes
normal weight |
type 1
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Type I or Type II Diabetes
often overweight |
type 2
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Type I or Type II Diabetes
anti-islet cell antibodies |
type 1
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Type I or Type II Diabetes
decreased blood insulin |
type 1
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Type I or Type II Diabetes
normal or increased blood insulin |
type 2
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Type I or Type II Diabetes
50% concordance in twins |
type 1
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Type I or Type II Diabetes
90-100% concordance in twins |
type 2
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Type I or Type II Diabetes
genetics: human leukocyte antigen D linked |
type 1
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Type I or Type II Diabetes
genetics: about 40% chance of inheriting from a first degree relative |
type 2
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Type I or Type II Diabetes
severe insulin deficiency due to pancreatic failure |
type 1
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Type I or Type II Diabetes
relative insulin deficiency |
type 2
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Type I or Type II Diabetes
B-cell depletion and/or failure |
type 1
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Type I or Type II Diabetes
inflammatory reaction early |
type 1
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Management for which type of diabetes
Diet control – Exercise – Insulin – Oral Medication - Blood Glucose Monitoring Urine Testing (“old school”) |
Diet control – type I and II
Exercise – Type I and II Insulin – for Type I Oral Medication -Type II Blood Glucose Monitoring Urine Testing (“old school”) |
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Lab tests
Fasting glucose: no caloric intake x8hrs what is normal? what is abnormal? --what does that tell you? |
N = 70-110
Abnormal: greather than 110 but less than 126mg/dl Impaired glucose tolerance: --if you have greater than 126 mg/dl on two separate occasions is diagnostic for diabetes. Draw 2 separate fasting glucose levels at separate times, that are both greater than 126 200 or greater = diabetes |
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Lab tests
Glucose Tolerance -Pt drinks a measured dose of glucose (75mg) -Blood samples obtained q30 min x 2hrs what is normal? abnormal? |
N = less than 140
Abnormal = greater than 139 but less than 200 Impaired glucose tolerance (IGT) greater than 200mg/dl + test for diabetes |
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Lab tests
what is now being used to Dx diabetes as of 2010) gold standard for diagnosing diabetes??? |
HbA1C
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Lab tests
HbA1C what is the risk for retinopathy what is high risk |
6.5% or greater is the cut off for risk of retinopathy
5.4% - 6.4% high risk |
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Lab tests
HbA1C is what? value of 6? 7? 5? |
on your red cell, there is a protein attractive to glucose and the glucose will stay attached to the red cell for 3 months. It tells you what your sugar in your blood has been over a 3 month period
-Stay under 6. if 6, glucose intolerant. If 7, you are a diabetic. If 5, your normal |
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Lab tests
Physician monitor Hgb A1C (Glycosylated) value needs to be ___ for a diabetic |
< 7
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How does insulin assist in providing energy for the body?
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insulin is needed to move glucose into most body tissues. a lack of insulin in diabetes from either a lack of production or a problem with insulin use at its cell receptor, prevents some cells from using glucose for energy
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What is meant by sliding scale insulin and how is it administered
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based on pts glucose level at that given time
Refers to a dosage of Regular Insulin to be given according to Blood Sugar results Example: “Cover” patient with Regular Humulin Insulin or Humalog according to the following: <150 = “O” coverage 151-250 = 2 U 251-350 = 4 U >350 , Call MD |
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Humalog
-type: -starts: -peaks: -finishes: |
rapid acting
5-15 min 45-60 min 3-4 hrs |
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Novolog
-type: -starts: -peaks: -finishes: |
rapid acting
10-20 60-90 3-5 hrs |
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Regular
-type: -starts: -peaks: -finishes: |
short acting
30 min 2 hrs 3-5 hrs |
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NPH
-type: -starts: -peaks: -finishes: |
intermediate acting
1-3 hrs 4-6 hrs 12-16 hrs |
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Lantus/Levemir
-type: -starts: -peaks: -finishes: |
long acting
1-2 hours NO PEAK 24 hrs |
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Why do pts have to take insulin when they are a Type I diabetic
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Because they have absolute insulin deficiency
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education for diabetics
why is it important to teach the peak for insulin? |
b/c it will tell you when the greatest potential for hypoglycemia can occur
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Illness, infection, and stress, can increase the need for Insulin
true or false |
true
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Diabetic Ketoacidosis
Pathophysiology -caused by what? resulting in what? what does insulin defificiency also affect in the body? |
Caused by an absent or inadequate amount of Insulin,
resulting in hyperglycemia & leads to a series of biochemical disorders. Insulin deficiency affects many aspects of the metabolism : carbohydrate, protein, & fat. -The amount of glucose entering the cells is reduced, & fat is metabolized instead of carbohydrate Free fatty acids are mobilized from adipose tissue, & ketone bodies are produced. |
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Diabetic Ketoacidosis
Only can happen in Type I or Type II diabetic |
type 1
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Diabetic Ketoacidosis
Ketone bodies escape into the blood & metabolic acidosis occurs, with lowering of serum bicarbonate, PCO2, & pH. The clinical picture is: |
hyperglycemia, water/lyte loss, acidemia & coma
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Diabetic Ketoacidosis
what happens to the urine? |
Large” urine or blood ketones are usually present for at least four hours before the total body’s acidity is increased (acidosis or DKA).
-urinating a lot, there is a change in potassium |
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Diabetic Ketoacidosis
Causes of DKA: |
Undiagnosed Type I Diabetes (somebody young, not old)
Untreated Diabetes Missed Dose of Insulin Illness (#1 cause of DKA. It is a stress which increases glucose) Infection –part of illness |
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Diabetic Ketoacidosis
What symptoms would the patient display |
Blood glucose levels from 300-800!
Serum ketones will be positive in blood Low serum bicarbonate (DO ABG, shows low serum bicarb and low pH) Low pH Abnormal K & Na levels (low) depending on hydration status (shift. Body is trying to conserve water because you are urinating. The body’s way to help itself is shift K out of the cell, and putting Na into the cell, to try to rehydrate it. serum sodium will get low. Serum K will go up. Kussmaul breathing (deep breaths to compensate for acidosis) long expiratory phase. Bodies mechanism to blow off CO2 “Fruity” odor to the breath Nausea & abdominal pain |
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Interventions / Treatment for DKA
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Restore circulating volume
Treat dehydration: 1 L NS first, then repeated, followed by 0.45% saline, when BS reaches 250 mg/dl, then 5%D/0.45% Treat hyperglycemia with IV Push Insulin (#1 thing we do first. NS will not lower glucose. It will hydrate. To lower glucose, you need insulin. And it is regular insulin only. Humalog and novolog can’t be given IVP. Correct electrolyte imbalances -Circulatory collapse is a killer |
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Interventions / Treatment for DKA
what do you give 1st? what is it based on |
Give IVP first , regular insulin
Based on serum glucose. Test. Sodium tells you what bag you are going to hang of NS. If potassium is low, the shift has not happened yet. If K is low, give supplement. If K is too high, give medications to off set it. |
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Which diabetic patient is at risk for DKA to occur
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TYPE 1 diabetics and most often starts from infection
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- complications associated with DKA:
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death occurs up to 10% of these cases . polyuria, polydipsia, Polyphagia, weight loss, vomiting, abdominal pain, dehydration, weakness, altered mental status, shock, and coma .
Kussmaul respirations (very deep and rapid respirations) cause respiratory alkalosis in an attempt to correct acidosis by exhaling carbon dioxide. |
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Diabetes
DIAGNOSING STARTS WITH ASSESSING FOR SIGNS & SYMPTOMS: |
Polyuria – increased urination*
Polydipsia – excessive thirst* Polyphagia – excessive hunger* Hyperglycemia Weight loss (can also be weight gain) Blurred vision Vaginal infections Fatigue Weakness Paresthesia Fruity odor to breath –only in type I who are heading into ketoacidosis Enuresis in children who are toilet-trained Slow wound healing |
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Type II
What type of pt is at risk for the development of this disease |
obesity and a higher than normal body mass index greatly increases the risk for diabetes (p. 1472)
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major risk factors for type 2 diabetes:
-testing should be considered in people 45 and older, particularly in those with a BMI of 25 people who are younger and are obese (BMI greater than 25 and have additional risk factors, such as: |
-first degree relative with diabetes
- inactivity, -members of a hish risk ethnic population (African American, Hispanic American, American Indian, asian American -delivery a baby weighing more than 9 pounds or have been diagnosed with GDM - hypertension (140/90) -HDL level less than 35 and/or triglyceride level greater than 250 mg/dL -have polycystic ovary syndrome -history of vascular disease |
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- Initial treatment associated with new diagnosis
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metformin (glucophage)as initial therapy for type II because it doesn’t induce wt gain and hypoglycemia, lost cost, few adverse effects, it is oral medication p. 1483
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- Oral medications that can be used in the Type II pt (general categories)
what do you have to educate on reguarding diet? usually administered every how many hours |
Prescribed for patients with Type II Diabetes, in addition to dietary changes (if they don’t eat, they can drop out their glucose = hypoglycemia)
Usually administered Q12 or Q24 hours |
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Teach the patient the signs & symptoms of Hyperglycemia vs. Hypoglycemia (hyper= polys) hypo = set of symptoms.
Teach that Insulin may be needed during stress, surgery, or if there’s an infection When a person is under stress, there is a increase glucose need -type I diabetic gets sick, they have a greater chance to go into ketoacidosis Stress the importance of ______________! |
COMPLIANCE
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- Oral medications that can be used in the Type II pt (general categories)
Sulfonylurea agents Meglitinide analogues . |
Sulfonylurea agents (stimulate insulin secretion from pancreatic beta cells and increase the number of sensitivity of cell receptor sites for interaction with insulin
Meglitinide analogues (lower blood glucose by triggering insulin secretion from pancreatic beta cells. designed to increase meal-related insulin secretion. |
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- Oral medications that can be used in the Type II pt (general categories)
Biguandies Alpha glucosidase inhibitors |
Biguandies – metformin (Glucophage) antihyperglycemia agents and insulin sensitizers. metformin (Glucophage) is the major drug in this class. it does not increase insulin secretion. instead, it decreases liver glucose production, thereby reducing fasting plasma glucose release and improves insulin receptor sensitivity.
Alpha glucosidase inhibitors (agents that prevent hyperglycemia by delaying absorption of carbohydrate from the small intestine. these drugs inhibit enzymes in the intestinal tract, reducing the rate of digestion of starches and the absorption of glucose. |
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- Oral medications that can be used in the Type II pt (general categories)
thiazolidinediones |
(antihyperglycemic agents and insulin sensitizers. they improve insulin sensitivity and reduce liver glucose production. they also improve insulin action in muscle, fat, and liver tissue by stimulating an enzyme receptor that regulates glucose and lipid metabolism
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- type of lab monitoring with the type II DM pt ( after meds started)
3 |
Home glucose monitoring –for type I, II, glucose intolerance
HbA1c - every 3-6 mo for monitoring and control Monitoring urine for kidney function and ketones |
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Lab values - Type 2
how do you check kidney function? |
Kidney function: looking for protein and glucose in the urine
Microalbuminuria (protein in urine) N = 0.2 -1.9 mg/dl > = early renal disease Ketones: (acetone bodies) Urine and blood Waste product of fat metabolism (fatty acid catabolism) Urine N = 0 Blood N = negative Abn urine & blood will be positive Should be no ketones in urine, if they have ketones, they broke down fat and muscle and they are metabolizing themselves to give energy |
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Type II
Microalbuminuria (protein in urine) N = = early renal disease |
Microalbuminuria (protein in urine)
N = 0.2 -1.9 mg/dl > = early renal disease |
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Ketones: (acetone bodies) Urine and blood
--What is it? Urine N = Blood N = Abn urine & blood will be positive |
Ketones: (acetone bodies) Urine and blood
--Waste product of fat metabolism (fatty acid catabolism) Urine N = 0 Blood N = negative Abn urine & blood will be positive Should be no ketones in urine, if they have ketones, they broke down fat and muscle and they are metabolizing themselves to give energy |
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- Nursing education that needs to be given to the newly diagnosed pt.
teach all pts with diabetes that tight control of blood glucose levels can prevent life shortening complications. |
:)
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-the initial phase of diabetic education involves teaching information necessary for anybody diagnosed with diabetes. survival information includes:
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simple info on Pathophysiology of diabetes
learning how to prepare and administer insulin, or how to take PO meds basic diet information monitoring blood glucose and ketones recognizing, treating, and preventing hypoglycemia and hyperglycemia sick day management where to buy supplies and how to store them when and how to notify their dr p. 1514 |
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Hypoglycemia:
- What is it |
blood sugar less than 60 mg/dL
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Hypoglycemia:
- what are the symptoms of this: You don’t just use a number. You use s/s and you treat based upon s/s |
- Sweating-main sign
- Tremor-main sign - Tachycardia –main sign - Palpitations - Nervousness - Headache –late sign - Lightheadedness - Double vision - Confusion - Irritability |
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Hypoglycemia:
This is not about numbers but about symptoms!! what causes the sweating, tremors, tachycardia, palpitations, and nervousness! |
When the blood glucose falls rapidly, the sympathetic nervous system is stimulated to produce ADRENALIN,
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Hypoglycemia:
how is this treated if the pt is alert |
-15 grams of glucose (B-D glucose tabs; Walgreens Glucose; Dextrosol etc - see your pharmacist and check the label to take the right amount to equal 15 grams of carb). This is the best treatment.
-6 Life Savers candy (if each is=2.5 g carb) -3/4 cup (175mL) Regular soda pop -1 tablespoon (15 mL) honey -1 tablespoon (15 mL) sugar dissolved in water -To sustain them, you need a carb and a protein (white bread and turkey, PB) milk and gram crackers are good -Retest blood sugar in 15 minutes and retreat if blood sugar is less than 75 mg/dl -Also retreat if symptoms persist regardless of blood sugar level -Once symptoms resolve, give a snack of protein & carbohydrate (cheese & crackers, crackers & peanut butter) |
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Hypoglycemia:
- How is this treated if the pt is has ALOC and is not alert -If patient is unconscious and unable to swallow, administer: hospital home |
* in the hospital or ER, give 25-50 cc’s of
D50% in water (given IVP, usually 1 amp) -50% dextrose * at home, administer Glucagon injection SQ or IM (it may take 20 minutes for this to work!) * Hospital protocol may indicate administration of BOTH D50% AND Glucagon; check policy! |
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glucagon does what ??
Glucagon can cause vomiting, so the Nurse takes precautions to prevent aspiration! These meds are temporary, so the Nurse administers a simple sugar, followed by a small snack or meal. The goal is to ?? |
converts liver glycogen to glucose, and therefore if elevates the patient’s blood sugar.
keep BS between 70-110 mg/dl |
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Macrovascular complications: major ones p. 1468
what is the most common complication?? what is the leading cause of death? |
cardiovascular disease is the most common complication.
Coronary artery disease, athersclerotic changes, abnormal blood clotting MI leading cause of death in diabetics Cardiomyopathy Left ventricle most affected Heart failure/CHF Hypertension (HTN) Cerebrovascular disease (in the brain –risk factor for stroke) Peripheral Vascular Disease (PVD) Infection with delayed wound healing patients with renal disease, indicatd by aluminuria, increases the risk for CHD and MI |
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Microvascular complications: major ones
Neuropathies |
Retinopathy- disease of the retina. They need to have an eye exam yearly to examine the optic nerve
Nephropathy-tissue of the kidney. Destroys inner function of glomerulus. Have BUN and CREAT and microalbumin in urine Neuropathy -Gastroparesis (delayed stomach empyting) –you see a patient that vomits, can’t keep food in stomach Neuropathic Cardiovascular changes –vessels of the hearts that swell, mediates plaque and clot formation Pain perception can be altered Orthostatic hypotension |
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Microvascular complications: major ones
-elevated glucose causes inflammatory diseases which causes the comborbid diseases There is a THICKENING of the capillary basement membrane, most prominent in the retina & glomerulus. Also, a decrease in migration of WBC’s to an area of injury. -diabetic has a decreased perception of pain because the nerves have been damaged -what does glucose do to cellular permeability |
increases cellular permeability so water can get into the cell
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Kidney failure
How does diabetes play a role in the development of this process |
diabetic nephropathy is a pathologic change in the kidney that reduces kidney function and leads to kidney failure.
chronic high blood glucose levels causes hypertension in kidney blood vessels and excess kidney perfusion. the increased pressure damages the kidney in many ways. the blood vessels become leakier, especially in the glomerulus. this leakiness allows filtration of larger particles (including albumin and other proteins) which then form deposits in the kidney tissue and blood vessels. deposits narrow the vessels, decreasing kidney oxygenation and leading to kidney cell hypoxia and cell death. these processes worsen over time, with blood vessels in the glomerulus becoming scarred and unable to filter urine from the blood, leading to renal failure. |
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glucagon does what ??
Glucagon can cause vomiting, so the Nurse takes precautions to prevent aspiration! These meds are temporary, so the Nurse administers a simple sugar, followed by a small snack or meal. The goal is to ?? |
converts liver glycogen to glucose, and therefore if elevates the patient’s blood sugar.
keep BS between 70-110 mg/dl |
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Macrovascular complications: major ones p. 1468
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cardiovascular disease is the most common complication.
Coronary artery disease, athersclerotic changes, abnormal blood clotting MI leading cause of death in diabetics Cardiomyopathy Left ventricle most affected Heart failure/CHF Hypertension (HTN) Cerebrovascular disease (in the brain –risk factor for stroke) Peripheral Vascular Disease (PVD) Infection with delayed wound healing patients with renal disease, indicatd by aluminuria, increases the risk for CHD and MI |
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Microvascular complications: major ones
Neuropathies |
Retinopathy- disease of the retina. They need to have an eye exam yearly to examine the optic nerve
Nephropathy-tissue of the kidney. Destroys inner function of glomerulus. Have BUN and CREAT and microalbumin in urine Neuropathy -Gastroparesis (delayed stomach empyting) –you see a patient that vomits, can’t keep food in stomach Neuropathic Cardiovascular changes –vessels of the hearts that swell, mediates plaque and clot formation Pain perception can be altered Orthostatic hypotension |
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Microvascular complications: major ones
-elevated glucose causes inflammatory diseases which causes the comborbid diseases There is a THICKENING of the capillary basement membrane, most prominent in the retina & glomerulus. Also, a decrease in migration of WBC’s to an area of injury. -diabetic has a decreased perception of pain because the nerves have been damaged -glucose increases cellular permeability so water can get into the cell |
:)
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Kidney failure
How does diabetes play a role in the development of this process |
diabetic nephropathy is a pathologic change in the kidney that reduces kidney function and leads to kidney failure. chronic high blood glucose levels causes hypertension in kidney blood vessels and excess kidney perfusion. the increased pressure damages the kidney in many ways. the blood vessels become leakier, especially in the glomerulus. this leakiness allows filtration of larger particles (including albumin and other proteins) which then form deposits in the kidney tissue and blood vessels. deposits narrow the vessels, decreasing kidney oxygenation and leading to kidney cell hypoxia and cell death. these processes worsen over time, with blood vessels in the glomerulus becoming scarred and unable to filter urine from the blood, leading to renal failure.
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Kidney failure
leaading cause? |
Diabetes is the leading cause of end stage Kidney failure and renal failure*** (before you get to kidney failure, you have renal insufficiency and as the glomerulus becomes injured by the glucose it will lead to renal failure. Monitor BUN and CREAT and microalbumin in the urine specimen. There should be no protein in urine. The protein cell is a big cell, it shouldn’t be ale to pass in the tubes and come out in the urine. You will see protein in the urine is when you have blood (protein is in your blood) in your urine and kidney disease starting, or w/ someone with hypertension and you will see small amounts of red cells
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Kidney failure
3 races that have the greatest risk 4 development |
Native Americans,
Hispanics African Americans |
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Kidney failure
Patho: |
High glucose levels cause hypertension in the kidney infrastructure (bld vessels) which in turn become damaged. The glomerulus is one of the most vulnerable kidney structures
Narrow vessels (leading to scarring) a decrease in oxygenation of kidney cells which leads to hypoxia and cell death Blood is not able to filtered, results equate to kidney failure |
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Kidney failure
Labs performed. (know your lab values for these) what kind of test do you do to check if your kidneys are having a problem? -protein -glucose -microalbumina -what do ace inhibitors do? |
UA –how do you know your kidneys are having a problem
Protein –should be none Glucose –should be none Microalbuminuria –first sign of kidney insufficiency. ACE inhibitors help preserve the kidney |
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Kidney failure
Blood study -what do you look at? |
Blood
BUN and Creat are assessed together to evaluate kidney function BUN can become elevated in dehydration states while the creat will stay in the normal range BUN and Creatinine will be elevated in kidney failure Creatinine N = F 1.1mg/dl M 1.2mg/dl BUN N = 10-20 mg/dl |
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- What type of medication precautions are instituted for pt’s who are on type 2 meds and need to have IV contrast dye?
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-Biguandies – Metformin (Glucophage) should be held for 48 hrs before and after usingcontrast material and surgical procedures requiring anesthesia
WHY????/ rationale: iodinated contrast materials can alter renal function and increase the risk for lactic acidosis. metformin therapy is restarted when renal function has returned to normal) |
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Metabolic syndrome
-What is it also called? -what is it? |
also called syndrome X,
is the simultaneous presence of metabolic factors known to increase risk for developing type 2 diabetes and cardiovascular disease. |
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Metabolic syndrome
factors include: |
-abdominal obesity: waist circumference of 40 inches or more for men and 35 inches or more for women
-hyperglycemia: elevated fasting blood glucose level 100mg/dL or more or on drug treatment for elevated glucose -hypertension: systole of 130 or more or diastolic BP of 85mg or more -dyslipidemia: triglyceride level 150 mg/dL or more or on drug treatment for elevated triglycerides |
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Metabolic syndrome
Combination of multiple risk factors Heterogeneous across ethnic/racial populations More common in men than women Prevalence increases with age |
Can affect children
Incidence has doubled in teen agers (12-19y/o) over the last decade Caucasian white males and Mexican American males who have the syndrome are at highest risk for the development of CHD |
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Metabolic syndrome
A condition which includes: |
Obesity (especially around the abdomen)
High Cholesterol (high LDL, high Triglycerides & low 'good' HDL) Inactive Lifestyle (No Exercise) High Blood Pressure (Hypertension) and High Blood Sugars (Pre-Diabetes, Type II Diabetes & Hyperglycaemia) Family History of Heart Disease, Stroke & Diabetes Health promotion and diabetes: know what pts can do to help themselves ex of metabolic syndrome : pt with abnormal blood fat levels and hypertension |
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Diet and Diabetes
Adult – |
total # of daily calories is individualized based on current/desired wt
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Diet and Diabetes
Children - |
total # of daily calories is individualized on the basis of the child’s age & growth expectations
- With the Child: * allow the child to participate in food choices * the child should always carry candy |
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-Diet and Diabetes
Balanced diet between |
fat, protein and carbs
Recommendations - Carbs = 60-70% (fruit ,veggies, whole grains, legumes, and low fat milk) - Protein = 15-20 % - Fat = less than 10% (to reduce risk of cardiovascular disease) - Fiber = 20 – 35 gm (pushing fiber up to 40-40g) –legumes, fiber rich cereals, fruits, veggies, and whole grain products |
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-Diet and Diabetes
You have to control the ______to control the diabetes* |
calories
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-Diet and Diabetes
With Type I, a meal plan is based on |
food intake & insulin therapy. avoid weight gain (developing insulin regiments that conform to the patients preferred meal routines, food preferences, and exercise patterns)
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-Diet and Diabetes
With Type II, a meal plan is based on |
toward weight reduction, & improved glucose & lipid levels (focus on lifestyle changes that reduce calories eaten and increase calories expended through physical activity
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-How does insulin assist in providing energy for the body?
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Lowers blood glucose levels by enhancing glucose movement across cell membranes and into the cells of many tissues where it can be used
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- What is meant by sliding scale insulin and how is it administered
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dosage of regular insulin to be given according to blood sugar results
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- What type of Insulin is given with the sliding scale
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regular humulin insulin or Humalog
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- Why do pts have to take insulin when they are a Type I diabetic
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Because their pancreas doesn’t produce insulin where type 2 produce insulin but their bodies target cells are resistant to it
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-What is Diabetic Ketoacidosis?
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Caused by an absent or inadequate amount of insulin resulting in hyperglycemia and leads to a serious biochemical disorders. Body doesn’t know it has enough sugar b/c glucose cant get into cell which is where reads the glucose level in the body, brain signals body to break down fat to release glucose. free fatty acids are mobilized and ketone bodies are produced, they escape in the blood and metabolic acidosis occurs, with lowering of serum bicarbonate, PCO2, and pH.
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What symptoms would the patient display with DKA?
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Large urine or blood ketones are present, blood glucose levels form 300-800, serm ketones will e positive abnormal K and Na levels (low) low serum bicarbonate and pH, Kussmaul breathing, fruity odor to breath, nausea and abdominal pain
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Diabetic Ketoacidosis
treatment |
restore circulating volume treat dehydration (1 L NS first, then repeated, followed by 0.45% saline, when BS reaches 250 then 5%d/0.45%, trat hyperglycemia with IV insulin, correct electrolyte imbalance
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Diabetic Ketoacidosis
- complications associated with? |
with hypokalemia number one cause of death
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-Major symptoms of diabetes mellitus type II
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usually in older adults and those who are obese (the greater amount of adipose tissue the greater amount of cellular resistance) begins with insulin resistance, polyuria, polydipsia and polphagia
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type 2
- Initial treatment associated with new diagnosis |
diet and exercise for 6 months and reevaluated is number one
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Oral medications that can be used in the Type II pt (general categories)
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sulfonylureans –ide ending, Biguadined (glucophage) Avandia
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- type of lab monitoring with the type II DM pt ( after meds started)
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LFT, BUN, Creat, HbA1C
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- Nursing education that needs to be given to the newly diagnosed pt.
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healthy diet, exercise, wt loss, management of hypertension, cholesteros and smoking cessation, teach pt the signs and symptoms of hyperglycemia vs. hypoglycemia (tachycardia, confusion and sweating) stress importance of compliance
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Dawn Phenomenon results from
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nighttime release of growth hormone that cause blood glucose elevations at about 5-6 am.
Managed by providing more insulin for the overningt period |
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Somogyi effect
what is it |
morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia,
managed by ensuring adequate dietary intake at bedtime and evaluatingthe insulin dose and exercise programs to prevent conditions that lead to hypoglycemia |
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GTT glucose tolerance test measures
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amount glucose level 30 min q 2 hr after meal
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Glycosylated Hgb tells what
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what sugars doing for past three months look at red blood cell shows if patient is complient with medication
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