Diabetes Flashcards
(130 cards)
COMPLICATIONS OF DIABETES
LEADING CAUSE OF:
Adult blindness
ESRD (including dialysis and transplantation)
Non-traumatic limb amputations
Other risk factors:
Death from heart disease 2-4x higher
Stroke 2-4x higher
>50% have HTN and hyperlipidemia
NORMAL GLUCOSE AND INSULIN METABOLISM - where is glucose transported to?
Insulin is produced in the β cells of the islets of Langerhans of the pancreas
Function is to regulate blood glucose
When BG is high, insulin promotes transport of glucose into tissues (skeletal muscles and adipose tissue). Excess is stored as glycogen in liver
Released in small increments throughout the day and increased with food intake
DIABETES MELLITUS - what happens to the cells?
YOUR BODY HAS TROUBLE MOVING GLUCOSE FROM BLOOD INTO THE CELL
THIS LEADS TO HIGH LEVEL GLUCOSE IN THE BLOOD AND NOT ENOUGH IN THE CELL
CELL NEEDS GLUCOSE TO PRODUCE ENERGY
NOT LETTING GLUCOSE ENTER THE CELL LEADS THE CELLS TO STAVE FOR ENERGY
what ARE CONSIDERED INSULIN-DEPENDENT TISSUES?
INSULIN
PROMOTES GLUCOSE TRANSPORT FROM THE BLOODSTREAM ACROSS THE CELL MEMBRANE TO THE CYTOPLASM OF THE CELL
CELLS BREAK DOWN GLUCOSE TO MAKE ENERGY
LIVER AND MUSCLE CELLS STORE EXCESS GLUCOSE AS GLYCOGEN
SKELETAL MUSCLE AND ADIPOSE TISSUE ARE CONSIDERED INSULIN-DEPENDENT TISSUES
CLASSIFICATIONS OF DIABETES: TYPE I
TYPE 1 DIABETES: BODY DOES NOT MAKE ENOUGH INSULIN
Formerly known as juvenile-onset diabetes or insulin dependent diabetes
5-10% of diabetics
Generally in people under 40 but can occur at any age
Absence of endogenous insulin
Autoimmune disorder
Exposure to virus
80-90% of β cell destruction before symptom onset
DM I SYMPTOMS (the Ps and one other)
POLYPHAGIA: GLUCOSE CANNOT GET INTO CELL, CELL STARVES FOR ENERGY, WEIGHT LOSS
GLYCOSURIA: BLOOD GETS FILTERED TO THE KIDNEY, GLUCOSE IN THE URINE
POLYURIA: WATER FOLLOWS GLUCOSE
POLYDIPSIA: DEHYDRATION AND THIRST FROM POLYURIA
CLASSIFICATIONS OF DIABETES: TYPE 2 - what ethnic groups?
TYPE 2 DIABETES
Formerly known as Non-insulin dependent diabetes or adult-onset diabetes
Endogenous insulin produced but inadequate amounts, tissue resistance or overproduction of glucose by the liver
90-95% of diabetics
Less frequently in children but incidents rising due to childhood obesity
Contributing risk factors that lead to insulin resistance:
Family hx, obesity, increasing age, certain ethnic groups (Hispanics, Pacific Islanders, Native Americans, African Americans, Asian Americans)
TYPE 2 DIABETES MELLITUS ONSET OF DISEASE - is it fast or slow?
GRADUAL ONSET
HYPERGLYCEMIA MAY GO MANY YEARS WITHOUT BEING DETECTED
OFTEN DISCOVERED WITH ROUTINE LABORATORY TESTING
AT TIME OF DIAGNOSIS
ABOUT 50% TO 80% OF Β CELLS ARE NO LONGER SECRETING INSULIN
AVERAGE PERSON HAS HAD DIABETES FOR 6.5 YEARS
CLASSIFICATION OF DM: PREDIABETES- # for fasting and after oral glucose test
Individuals who are at an ↑ risk for developing diabetes
They have impaired glucose tolerance (IGT), impaired fasting glucose (IFG) or both
Impaired glucose tolerance – 140-200 mg/dL 2 hours after an oral glucose tolerance test (OGTT). Normal is <140
Impaired fasting glucose – 100-125 mg/dL (normal < 100)
Individuals should have BG and HbA1C checked regularly
Watch for symptoms of diabetes (fatigue, frequent infections, non-healing wounds)
Advise to lose weight, exercise and make healthy food choices to prevent diabetes
DIABETES: DIAGNOSIS AND MONITORING - how does Hba1c measure glucose?
FBG >126 mg/dL
OGTT >200 mg/dL
HbA1c >6.5
In 2010, the ADA recommended the use of *HbA1c for diagnosing diabetes. Advantages: fasting is not required. More accurate picture of glucose control over time (normal Hba1c < 6.55)
Classic Sx of hyperglycemia + random plasma glucose => 200 mg/dl
Hyperglycemia with 3 Ps (polyuria, polydipsia, polyphagia) & a FBG > 126, confirmed by repeat testing x1 = usually no more tests are needed
- Hba1c (glycohemoglobin) measures the % of hg on a RBC that is coated with glucose. Measures the average BG over the past 2 to 3 months. The higher the number, the poorer the BG control
GOOD GLUCOSE CONTROL - what should BG and HbA1c be?
Euglycemia can delay the onset and slow the progression of retinopathy, nephropathy, neuropathy.
Maintain a mean BG of 155 and a HbA1c of <7.0 will reduce risk of developing micro and macrovascular diseases
For every % point ↓ in Hba1c, there was a 35% reduction in risk for kidney and eye complications, but not cardiac
METABOLIC SYNDROME
A collection of risk factors that increases an individual’s chance of developing HTN, cardiovascular disease, stroke and diabetes.
EDUCATION ON NUTRITION
Can use the food pyramid but new method is “myplate” introduced by Michelle Obama
For every Kg lost, a diabetic gains 3 months of life.
Avoid alcohol
high in calories and no nutritional value
leads to hypertriglyceridemia
liver damage
Etoh consumption during fasting state:
Inhibits gluconeogenesis
Altered CNS further contributes to hypoglycemia unawareness
Delayed recovery from hypoglycemia in DMI
Lifestyle change – Difficult to make changes after years old habits
Drug therapy
TYPES OF INSULIN - Rapid acting - ex (a rapid lisp is novel)
Rapid acting
Aspart (Novolog), Lispro (Humalog)
INSULIN FACTOIDS
Regular insulin and ..logs = always clear solution
NPH and protamine containing insulins are cloudy; preparations have additives of zinc, protamine and acetate buffer
Premixed insulin (short/rapid acting with intermediate acting) What are the benefits vs drawbacks?
MIXING AND ADMINISTERING - clear before cloudy
Mixing
Which do you draw up first and why?
Rapid or short-acting first (clear solution) then intermediate (cloudy) or long-acting
This is to prevent contamination of intermediate/long acting from contaminating short acting
Administering
Sites – Rotate injection sites within a particular area ½ to 1” apart. Fastest absorption is from the FAT in the abdomen (not muscle), then arm, then thigh and last buttock.
INSULIN REGIMEN: THINKING LIKE A PANCREAS- Basal-bolus regime (just rapid at meals and long acting all day)
Basal-bolus regimen
Regimen that closely mimics endogenous insulin production
Uses rapid or short acting (bolus dose) insulin at meal time and intermediate or long acting (basal dose)
CONSIDERATIONS - TSA
If exercising, do NOT inject in the thigh
Assess insulin administration barriers:
Neuropathies
Visual and motor deficits
When injecting prefilled insulin syringe, gently roll in palm 10-20x to warm insulin and resuspend particles
Alcohol swabs – not necessary at home
What about traveling with insulin?
***on test - According to TSA website, notify TSA officer that you have diabetes and are carrying insulin. Insulin pumps and supplies must be accompanied with insulin, and must be clearly labeled.
INSULIN STORAGE - temp, and how long?
Insulin vials and pens may be kept at room temperature up to 4 weeks as long as it’s not < 0 degrees or >86F degrees
INSULIN
ADMINISTRATION OF INSULIN
ABSORPTION IS FASTEST FROM ABDOMEN, FOLLOWED BY ARM, THIGH, AND BUTTOCK
ABDOMEN IS OFTEN PREFERRED SITE
DO NOT INJECT IN SITE TO BE EXERCISED
ROTATE INJECTIONS WITHIN AND BETWEEN SITES
PROBLEMS WITH INSULIN THERAPY - what about fat?
HYPOGLYCEMIA
ALLERGIC REACTION
LIPODYSTROPHY
INSULIN COMPLICATION: SOMOGYI EFFECT
A unique combination of hypoglycemia early morning (2am to 4am) and rebound hyperglycemia upon waking up
Due to too much evening insulin causing counterregulatory hormones (epinephrine, GH, cortisol, glucagon) release which stimulate lipolysis, gluconeogenesis, glycogenolysis → hyperglycemia
DAWN PHENOMENON - and what hormones cause it?
(dawn grows)
Hyperglycemia also present upon awakening
Due to 2 counterregulatory hormones (growth hormone and cortisol). GH & cortisol oppose insulin causing glucose to rise
DRUG THERAPY: ORAL AGENTS - Sulfonylureas - what do they do? (cooking)
(sulfur pancakes)
Know major classifications, where they work and timing of the oral agents
Sulfonylureas – stimulates pancreas to produce more insulin
