Flashcards in Exam 3: Diabetes Deck (106):
Percentage of the US population affected by diabetes
8.3% (25.8 million people
Risk factors for getting DM (8)
- Parent, brother, sister with diabetes
- Gestational diabetes / gave birth to baby with high birth weight
- Pre-diabetes (FBC of 100-126)
- High BP
- Abnormal Cholesterol levels
Abnormal cholesterol levels that put a person at risk for DM (3)
LDL > 100
Function of the pancreas as an exocrine gland
Releases digestive enzymes
Function of the pancreas as an endocrine gland
Beta cells secrete insulin
How does glucose enter the bloodstream? (3 ways)
- Intestinal absorption
- Glycogenolysis in the liver
- Gluconeogenesis (Protein catabolism)
What is glucose used for... in tissues?
• CO2 + H20 + E
What is glucose used for... in the liver?
Glycogenesis (glycogen formed)
What is glucose used for... in energy storage? (2)
- Converted to fat
- Stored as glycogen in muscles
When is glucose excreted in urine?
BS level exceeds 200
Roles of insulin (5)
o Transports and metabolizes glucose for energy
o Stimulates the storage of glucose in the liver (Glycogenesis)
o Enhances the storage of fat in adipose tissue
o Transports amino acids and glucose into the cells
o Inhibits the breakdown of stored glucose, protein and fat
Constant level of blood sugars occurs in fasting state due to what two factors?
• Pancreas releases insulin
• Pancreas releases small amounts of glucagon (Glycogenolysis)
When does glyconeogenesis occur?
After 8-12 hours without food
Pathophysiology of DM Type 1
- MAIN THING
- Three physiological results
- MAIN RESULT
- MAIN THING: Destruction of Beta cells
1) Means that glucose is not stored as glycogen
2) Glycogenolysis and gluconeogenesis occur unrestrained
3) Fat breakdown occurs
- MAIN RESULT: Hyperglycemia
Pathophysiology of DM Type 2
- Main thing (2)
- Main result
- MAIN THING: Insulin resistance and / or decreased production of insulin
- MAIN RESULT: Hyperglycemia
Usually a DM2 patient would be started on lifestyle changes before any medication is introduced.
What patient would have lifestyle changes AND medication started right away?
A patient who also has cardiac problems
Length of onset: DM1 vs DM2
DM1: Rapid onset
DM2: Slow onset
What does "insulin resistance" mean?
- Insulin resistance: Cells are not responsive to stimulating glucose uptake
What is the body's initial response to insulin resistance?
What eventually occurs?
Insulin levels will rise to compensate
Eventually, body can't produce enough insulin: Glucose rises.
DM Diagnosis: Fasting Blood Glucose #
126mg/dL or higher
DM Diagnosis: Random glucose level #
200 mg/dL or higher on more than one occasion
DM Diagnosis: Hemoglobin A1C #
>6.5 or 7
Cause of hyperglycemia (4)
- Too much food
- Too little insulin or DM med
Onset of hyperglycemia
- May progress to diabetic coma
Sxs of hyperglycemia
- Extreme thirst
- Frequent urination
- Dry skin
- Frequent urination
- Blurred vision
- Decreased healing
Why does a hyperglycemic patient experience hunger?
Becasue not enough glucose actually gets into cells - extreme hunger
How often should you check blood sugar for Type 1 DM?
2-4x per day
How often should you check blood sugar for Type 2 DM?
2-3x per week, with one two hours post prandial
What type of insulin is used for fractionals
Regular insulin always
What type of fluids should you use with hyperglycemic patients?
Hypotonic or Isotonic
CHO - PROTEIN - FAT
percentages for diabetic patients
Why would you advise a DM patient to increase fibers?
Soluble fibers help control glucose because they slow absorption between the intestines
Oral meds for type 2 DM: For insulin resistance (general category)
Oral meds for type 2 DM: For decreased insulin production
Examples of antihyperglycemic agents (5)
Examples of hypoglycemic agents (4)
Goals of DM drug therapy - insulins
- Blood sugar at 70-110
- Px complications
- Px hypoglycemia
Contraindication of Insulin
- TIME: Rapid acting (clear)
- ONSET: 10-15 minutes
- PEAK: 1 hour
- DURATION: 3 hours
Regular (R) Insulin
- TIME: Immediate acting (cloudy)
- ONSET: half hour to hour
- PEAK: 2-3 hours
- DURATION: 4-6 hours
(Humulin "N" or "L" (Lente))
- TIME: Intermediate acting
- ONSET: 3-4 hours
- PEAK: 4-12 hours
- DURATION: 16-20 hours
- TIME: Long-acting (clear)
- ONSET: 1 hour
- PEAK No peak
- DURATION: 24 hours
Rapid reduction of blood sugar
R Insulin indication
Works on the immediate meal: Administer 20-30 minutes before a meal
Give after meals helps replace basal insulin
Controls FPG (Fasting Plasma Glucose)
- TIME: Long acting (cloudy)
- ONSET 6-8 hours
- PEAK: 12-16 hours
- DURATION: 20-30 hours
Enables LT baseline insulin levels; still need to add insulin at mealtimes with separate needle.
Which insulin should you NOT mix with other insulins?
Insulin percentage breakdown
70/30 insuiln: 70% NPH and 30% regular
What type of insulin can be given IV?
ONLY regular insulin
How is most of the insulin administered?
Why should you rotate sites with subQ insulin injections
Lipo-atrophy can develop (gets hard, doesn't absorb well)
Mixing types of insulin:
Clear to cloudy
(Regular first, then NPH in syringe)
Cause of hypoglycemia (3)
- Too little food
- Too much insulin or DM meds
- Extra activity
Onset of hypoglycemia
- Sudden; may progress to insulin shock
Sxs of hypoglycemia (10)
**MOSTLY NERVOUS SYSTEM
- Fast heartbeat
- Imapired vision
- Weakness / fatigue
Old saying for DM - hyper vs hypoglycemia
Cold and clammy, you need candy
Hot and dry, blood sugar is high
If your DM pt is comatose, what is your priority?
To maintain an airway
If you can't tell if a pt is hypo- or hyperglycemic...
ERR ON THE SIDE OF HYPOGLYCEMIC
Clinical picture of a patient with mild hypoglycemia (6)
Anxiety or drowsiness
Clinical picture of a patient with moderate hypoglycemia (6)
Blurred, impaired or double vision
Irritation / confusion
Clinical picture of a patient with severe hypoglycemia (4)
Unable to take oral feeding
What do you give a hypoglycemic patient
15 grams of CHO
DIabetic ketoacidosis is secondary to...
Clinical picture of diabetic ketoacidosis
Why is a ketoacidosis patient at risk for hypokalemia
- K+ can move from intracellular to extracellular to compensate for acidity
- Can get worse as treatment progresses
Blood sugar of a ketoacidotic patient
Respirations of a ketoacidotic patient
Fluid and electrolytes in a ketoacidotic patient
Loss of both
Medical management of DKA
- Insulin IV
- NS or 0.45 NS for dehydration (as much as 500-1000mL over an hour)
Mortality rate from ketoacidosis
Clinical picture of HHNS (4)
• Altered senses, decreasd LOC
What does HHNS stand for?
Hyperglycemic Hyperosmolar Nonketotic Syndrome
Cause of HHNS
Usually non-compliance with treatment
Nursing assessment of HHNS: Blood sugar
Nursing assessment of HHNS: RR, pH, ketones
How do you prevent HHNS?
Sick Day Rules
Six Sick Day Rules
1. Take insulin / oral medications as usual
2. Test your blood sugar q 3-4 hours (if more than 200, test for ketones)
3. Report a blood sugar reading greater than 300
4. Eat small, frequent meals
5. If you are vomiting or have diarrhea, have a half of a can of cola, juice or broth every half hour
6. Report nausea, vomiting or diarrhea to your health care provider.
DM Complications (7)
1) Complications with insulin therapy
4) Macrovascular issues
5) Microvascular issues
Macrovascular issues with DM (3)
What is unique with CAD in DM patients?
Typical ischemic symptoms (early warning sxs) might be absent, because these patients develop an autonomic neuropathy
MIs and DM patients
Higher incidence / more complications / higher mortality with diabetic patients
Correlation of HTN and DM
60% od DM patients have high BP
DM patients and CVD
Higher incidence of strokes, CVAs
(3x more likely to have a stroke than a non-DM patient)
PVD and DM: Amputations
600,000 amputations with DM patients
Prophylactic meds for Macrovascular issues in DM patients (5)
o An aspirin a day
o beta blocker
o ACE inhibitor or Ca channel blocker
o and a statin
Microvascular issues with DM (2)
What can retinopathy lead to?
Who is at risk for neuropathies?
Patients with longstanding DM (25+ years)
What is a big risk with neuropathies?
Peripheral sensorimotor nephropathy -- affects distal portions of the nerves in the lower extremities
Autonomic neuropathy: Systems affected (4)
DKA versus HHNK: Caused by which type of diabetes?
DKA: Type 1
HHNK: Type 2
DKA versus HHNK: Serum glucose
HHNK: Often >1,000
DKA versus HHNK: Arterial pH
DKA versus HHNK: Serum and urine ketones
DKA: Positive for both
HHNK: Negative for both
DKA versus HHNK: Onset
DKA versus HHNK: Cause
DKA: Lack of insulin --> Breakdown of fats
HHNK: Inadequate insulin, but enough to prevent the breakdown of fats
DKA AND HHNK: Clinical assessment
- Dry skin and mucous membranes
- Decreased skin turgor
- Altered LOC
DKA versus HHNK: Breathing
DKA: Kussmaul's respirations
HHNK: Regular and shallow
DKA versus HHNK: Mortality
HHNK: Near 50%
Diabetes insipidis is caused by a disorder of the ______
What causes diabetes insipidus?
Head trauma or neurosurgery -- damage to insipidus
Sxs of Diabetes insipidus
(Can urinate 4-16 L per day)
Treatment for Diabetes Insipidus (3)
o Replace fluids
o Is & Os
o Diet: High sodium, high potassium