Exam 3: Diabetes Mellitus Flashcards
Tropic system
Hormones are stimulated by other hormones.
Diabetes Mellitus
Is a multisystem disease affecting carbohydrates, protein and fat metabolism, related to abnormal insulin production and impaired insulin utilization.
Insulin is produced by
By beta cells of the islets of langerhan of the pancreas
The effect of insulin is to
Decrease blood sugar.
Counter Regulatory Hormones Opposed to Insulin include
o Glucagons
o Epinephrine
o Growth Hormone
o Cortisol
Too much cortisol can lead to
Hyperglycemia
Type I Diabetes Mellitus
Formerly known as “juvenile onset” or “insulin dependent”, most often occur to people who are under 30 years old (11-13)
Pathophysiology of Diabetes Mellitus Type I
o Progressive destruction of pancreas B cell d/t autoimmune process
o Develop when the persons pancreas can no longer produce insulin
Type II Diabetes Mellitus
- Most prevelant type of diabetes
- Usually occurs in people over 40 years old
- Known as “adult onset”
Pathophysiology of Diabetes Mellitus Type II
o Type 2 produces some endogenous insulin.
o The insulin produced is insufficient for the needs of the body or is poorly utilized by the cell or the tissue.
3 Metabolic Abnormalities of Diabetes Mellitus Type II
- Insulin resistance.
- Decreased ability of the pancreas to produce insulin.
- Inappropriate glucose production by the liver.
Gestational Diabetes
Diabetes that develops during pregnancy (24-28 gestation)
Secondary Diabetes
Secondary Diabetes
Diabetes Mellitus due to treatment that produces diabetes. E.g Parenteral nutrition, prednisone and Dilantin.
Clinical Manifestations of Diabetes Mellitus Type I
- Polyuria
- Polydipsia
- Polyphagia
- Weight loss
- Weakness and fatigue
Diagnostic Studies for DM
- Fasting plasma glucose
- Random or casual plasma glucose
- 2 hour OGTT (oral glucose tolerance test)
- Glycosylated hemoglobin
Collaborative Care Goals for DM
- Reduce symptoms
- Promote wellbeing
- Prevent acute complications of hypoglycemia
- Delay onset and progression of long-term complications
Focus of Collaborative Care for DM
- Patient Teaching: anticipatory guidance
- Nutritional Therapy
- Drug Therapy: Insulin & Oral hypoglycemic
- Exercise
- Self-monitoring of blood glucose
2 Types of Glucose Lowering Agents
- Insulin
2. Oral hypoglycemic
Exogenous Insulin
• Is required for the management of type I diabetes.
• May be given with type II diabetes if glucose cannot be controlled especially during periods of severe stress, such as illness or surgery.
(Stress releases hormones that can stimulate glycolysis for energy = increased glucose in blood. “Fight or flight” response.)
Types of Insulin
- Rapid Acting Insulin (Humolog, Novolog)
- Short Acting Insulin (Regular)
- Intermediate Acting Insulin (NPH/Lente)
- Long Acting (ultralente)
- Long Acting (lantus)
Onset, Peak and Duration: Rapid Acting Insulin
Onset: 15 min
Peak: 60-90 min
Duration: 3-4 hours
Onset, Peak and Duration: Short Acting Insulin (Regular)
Onset: 1/2 - 1 hour
Peak: 2-3 hours
Duration: 4-6 hours
Onset, Peak and Duration: Intermediate Acting Insulin
Onset: 2 hours
Peak: 6-8 hours
Duration: 12-16 hours
Onset, Peak and Duration: Long Acting Insulin (ultralente)
Onset: 2 hours
Peak: 16-20 hours
Duration: 24+
Onset, Peak and Duration: Long Acting (lantus)
Onset: 1-2 hours
Peak: none
Duration: 24+
What are the oral hypoglycemic agents used to treat DM?
- sulfonyloreas (1st generation: orinase, 2nd generation: micronase/glucotrol)
- Meglitinides (prancing)
- Biguanides (metformin/glucophage)
- Alpha glucosidase inhibitors
- Thiazolidinediones (avandia and something else)
Sulfonyloreas
Orinase, Micronase, Glucotrol, Glyburide
Increases insulin production
Meglitinides
Prandin
Increases insulin production in the pancreas.
Biguanides
Metformin/Glucophage
Decreases glucose production by the liver.
Increases insulin sensitivity at the tissue.
Alpha Glucosidase Inhibitors
Acarbose
- Decreases absorption of carbohydrates in the small intestine.
- Taken with the first bite of each meal
Thiazolidinediones
Actos, Avandia
- Insulin sensitizers
- Increases glucose uptake in muscle; decreased endogenous glucose production.
Nutritional Therapy for DM
- Person can eat the same food as non diabetics
- Meal planning based on the individuals food intake and balance with insulin and exercise
- Reduce total fat, saturated fat and simple sugar
- Spacing meal
- Weight reduction 5-7% to improve glycemic control
Exercise for DM
- Increases insulin sensitivity thus lowering blood glucose level
- Regular reduces triglyceride in LDL
Patient using hypoglycemic agent should schedule exercise
- 1 hour after meal or have 10-15 g carb before exercise
- Small carb snacks every 30 min during exercise.
Nursing Therapeutics for DM: Health Promotion
Routine screening for diabetes for all over weight adults over 45
Nursing Therapeutics for DM: Acute Interventions
o Control hyperglycemia in times of stress
o If glucose is greater than 240 mg/dL, urine should be tested for ketones
o Do not stop hypoglycemic agent/insulin during times of illness
o Patient on oral hypoglycemic can be given insulin 48 hours prior to surgery
o Monitor for s/s of hypoglycemia
Nursing Therapeutics for DM: Ambulatory or Home Care
o Promote self care
o Provide emotional support
o Patient to wear medical identification
Complications of DM
Arise from events associated with hyperglycemia and insufficient insulin o DKA (diabetic ketoacidosis) o HHNS (Hyperosmolar Hyperglycemia Non Ketotic Syndrome)
Diabetic Ketoacidosis is caused by
Profound deficiency of insulin.
DKA is characterized by
o Hyperglycemia
o Ketosis
o Acidosis
o Dehydration
DKA: Clinical Manifestations
- Dehydration
- Tachycardia
- Lethargy
- Anorexia
- Kussmaul respirations: remove CO2 d/t increased ketones (decrease acidity)
- Acetone breath
- Arterial blood glucose above 250 mg/dL
- PH lower than 7.35
DKA: Collaborative Care
- IV administration of rapid acting insulin
- IV fluids, electrolyte replacement, I&O
- Labs: glucose, ketones in urine
- ECG, Assess CV and Respiration
- Ensure patent airway
- O2 therapy
- IV fluid resuscitation with 0.9% NaCl 1L/hr until BP is stable and urine output of 30-60 ml/hr
- Insulin drip 0.1 u/kg/hr
- Potassium to correct hypokalemia/Bicarb pH < 7.0
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HHNS
- Is life threatening
- Can occur in the patient with DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia osmotic diuresis and ECF depletion.
- Occurs with patient diagnosed of type II diabetes Mellitus.
Collaborative Care for HHNS
- IV administration of 0.9% or 0.45% NaCl rate dependent on cardiac status
- Regular insulin given IV
- When blood sugar falls approximately 250 mg/dL, IVF is given with glucose to prevent hypoglycemia.
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Other complications of DM
- Hypoglycemia
- Blood glucose drops to < 70 mg/dl
- Nephropathy
- Neuropathy
- Angiopathy
- Retinopathy
Management of Hypoglycemia for a Conscious patient
o Administer 15-20g of quick carb (juice) 6-8 oz, soda, life saver, syrup or honey
o Repetition of tx 15 min if no improvement
o Long acting carb once glucose is above 70
Management of Hyperglycemia for an Unconscious patient
o SQ or IM of 1 mg glucagons
o IV 50 mL of 50% glucose (need to make sure it is not infiltrated. Can be necrotizing.)
What is a normal blood glucose?
70-120 mg/dL
Insulin: Action
Promotes transportation of glucose from the blood to the cell -> decreases glucose in blood stream.
Why is insulin called the anabolic/storage hormone?
Increased insulin after a meal leads to the conversion of glucose to glycogen in liver and muscle.
Gluconeogenesis is then inhibited leading to an increase in fat deposition of adipose tissue and increased protein synthesis.
What tissues are dependent on insulin?
Skeletal muscle and adipose tissue
The fall in insulin level during normal overnight fasting facilitates
The release of stored glucose from the liver, protein from muscle and fat from adipose tissue.
Counter regulatory hormones to insulin work by
- increasing blood glucose levels by stimulating glucose production and output by the liver
- decrease the movement of glucose into the cells
Glucagon
Made in alpha cells in the pancreas
Stimulates glycolysis and gluconeogenesis to increase glucose levels.
Epinephrine
Released in response to stress -> fight or flight
Your body needs energy during fight or flight, energy comes from glucose so the result will be an increase in glucose levels.
Cortisol
Natural corticosteroid from adrenal cortex released in response to stress.
How do corticosteroids work?
- Increase glucose levels by hepatic gluconeogenesis and inhibits protein synthesis.
- Also, decreases glucose in fasting state and causes free fatty acids (comes from the breakdown of fatty acids)
How is diabetes related to genetics?
Related to human leukocyte antigens (HLA).
Idiopathic diabetes
Form of type 1 diabetes that is INHERITED
-Hispanic, African or Asian ancestry
Latent autoimmune diabetes
- Slowly progression autoimmune form of type 1.
- People over the age of 35 and NOT obese
What causes polyuria in diabetes Mellitus?
D/t increased blood glucose and release of more glucose from the kidneys. (Water wants to follow glucose so the release prevents water reabsorption)
What causes polydipsia in diabetes Mellitus?
D/t decreased water reabsorption -> cellular dehydration
What causes polyphagia in diabetes Mellitus?
D/t having no glucose in the cells -> cellular starvation
What causes weight loss in diabetes Mellitus?
D/t cell starvation.
Fat and protein are used as an energy source.
What causes weakness and fatigue in diabetes Mellitus?
D/t not having energy to utilize.
What happens during the early stages of insulin resistance?
Hyperinsulinemia d/t pancreas responding to high glucose and secreting more insulin.
How do adipokines lead to diabetes Mellitus?
Adipokines cause chronic inflammation -> insulin resistance -> Type II DM
Clinical Manifestations of DM Type II
May have same symptoms as Type I
- Fatigue
- Recurrent infection
- Prolonged wound healing
- Visual changes
- Chronic O2 deficiency
- Neuropathy
What causes visual changes in diabetes Mellitus?
Lens of the eye needs proteins to stay clear -> w/o protein the lean becomes opaque.
This happens because the body is using protein as energy source because it cannot use glucose d/t insulin insufficiency.
What causes chronic O2 deficiency in DM?
D/t unmanaged glucose sticking to hemoglobin as manifested by clubbing.
How does Cushing’s syndrome lead to DM?
Increased release of cortisol
How does pancreatitis lead to DM?
Decreased insulin production.
How can hyperthyroidism lead to DM?
Increased GI glucose absorption from hepatic gluconeogenesis
Prediabetes: Impaired fasting glucose is
100-125 mg/dL
Prediabetes: Impaired glucose tolerance test
140-199 mg/dL
Fasting Plasma Glucose
No caloric intake for at least 8 hours.
If >126 mg/dL -> Diabetes
Random or Casual Plasma Glucose
Any time of day without regard to the time of last meal.
If >200 + 3 P’s -> Diabetes.
2 Hour Oral Glucose Tolerance Test
- Uses glucose load of 75 g -> Patient drinks juice and then blood glucose level is measured during a 2 hour period.
- If it remains >200 mg/dL -> Diabetes.
What are factors that can falsely elevate OGTT?
Severe restriction of carbohydrates and activity like bed rest, acute illness and medications (contraceptives and corticosteroids)
HgA1C
Measures the amount of glucose attached to hgb in its lifetime.
Shows overall glucose control for the past 90-120 days.
For patients with diabetes, the ideal A1C goal is
<7%
HgA1C indicates diabetes when
Levels are >6.5%.
Basal insulin
Keeps blood glucose at a consistent level during periods of fasting.
Bonus insulin
Taken at meal time to keep blood glucose under control following a meal.
Insulin storage considerations
Left at room temperature for up to 4 weeks unless the room temperature is higher than 86 degrees F.
Extra should be stored in the refrigerator.
Lipodystorphy
A condition that produces lumps and dent sin the skin from repeated injection in the same spot.
Somogyi Effect
-A rebound effect in which an overdose of insulin induces hypoglycemia that leads to rebound hyperglycemia.
-Counter Regulatory hormones are released, stimulating lipolysis, gluconeogenesis, glycolysis which in turn produce rebound hyperglycemia and ketosis.
(Growth hormone, epinephrine, cortisol and glucagon are secreted)
Dawn Phenomenon
- Hyperglycemia in the morning.
- Counterregulatory hormones are released during morning hours which lead to hyperglycemia -> growth hormone and cortisol are secreted.
DM Patients undergoing surgery or radiography involving contrast medium are instructed to
Temporarily discontinue metformin before surgery or the procedure
Hypoglycemia
Occurs when there is too much insulin.
Blood glucose drops to <70 mg/dL
Affects mental functioning.
Hypoglycemia can mimic
Alcohol intoxication
Nephropathy
Microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney.
Neuropathy
Nerve damage that occurs because of the metabolic derangement associated with DM
Angiopathy
Organ disease from damage to blood vessels secondary to chronic hyperglycemia
Retinopathy
Refers to the process of microvascular damage to the retina as a result of chronic hyperglycemia, presence of nephropathy and HTN in patients with DM
