Diabetes Mellitus Flashcards
What is Normal insulin metabolism
Produced by B -cells in islets of Langerhans of Pancreas
Released continuously into bloodstream in small increments with larger amounts released after food
Stabilizes glucose level in range of 70 to 120 mg/dL
Normal Insulin Secretion
Type 1 Diabetes Mellitus Etiology and Pathophysiology
Autoimmune destruction of β-cells
Total absence of insulin
Genetic predisposition and viral exposure
Idiopathic diabetes
Latent autoimmune diabetes in adults (LADA)- Older adult who are not obese
Type 1 Diabetes Mellitus Onset of Disease
Autoantibodies are present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin—then rapid onset with ketoacidosis
Necessitates insulin
Patient may have temporary remission after initial treatment
Type 2 Diabetes Mellitus
Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM)
Most prevalent type (90% to 95%)
Risk factors: overweight, obesity, advancing age, family history
Type 2 Diabetes Mellitus Etiology and Pathophysiology
Pancreas continues to produce some endogenous insulin
Insulin insufficient or poorly utilized
Multiple etiologic factors
Obesity is greatest risk factor
Genetic component increases insulin resistance and obesity
Four major metabolic abnormalities
Insulin resistance
Decreased insulin production by pancreas
Inappropriate hepatic glucose production
Altered production of hormones and cytokines by adipose tissue (adipokines- They interfere with absorption of glucose)
Type 2 Diabetes Mellitus Onset of Disease
Gradual onset
Hyperglycemia may go many years without being detected
Many times discovered with routine laboratory testing
Altered Mechanisms in Type 1 and Type 2 Diabetes
Type 2 Classic symptoms
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue
Type 2 Nonspecific symptoms
Classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candidal infection
Prolonged wound healing
Visual changes
Diagnostic Studies
Hemoglobin A1C level: 6.5% or higher
Fasting plasma glucose level: higher than 126 mg/dL
Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)
Classic symptoms of hyperglycemia with random plasma glucose level of 200 mg/dL or higher
Fructosamine
Reflects glucose levels past 1-3 weeks
Autoantibodies
Hemoglobin A1C test
Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: less than 6.5%
Goals of diabetes management
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications
Need to maintain blood glucose levels as near to normal as possible
Patient teaching
Nutritional therapy
Drug therapy
Exercise
Self-monitoring of blood glucose
Diet, exercise, and weight loss may be sufficient for patients with type 2 diabetes
All patients with type 1 require insulin
Insulin Categorized according to onset, peak action, and duration
Rapid-acting
Short-acting
Intermediate-acting
Long-acting
Examples of rapid acting
Humalog
Novalog
Apidra
Examples of short acting
Humalin R
Novalin R
Examples of Intermediate Acting
NPH
Humulin N
Novolin N
Examples of long acting
Lantus
Levemir
Rapid acting onset, peak, duration
onset: 10-30 minutes
peak: 30 minutes- 3 hours
duration: 3-5 hours
Short acting onset, peak, duration
Onset: 30 min- 1 hour
Peak: 2-5 hours
Duration: 5-8 hours
Intermediate acting onset, peak, duration
Onset: 1.5-4 hours
Peak: 4-12 hours
Duration: 12-18 hours
Long acting onset, peak, duration
Onset: 0.8-4 hours
Peak: No pronounced peak
Duration: 24+ hours
Rapid-acting (bolus)
Lispro, aspart, glulisine
Onset of action 15 minutes
Injected within 15 minutes of mealtime
Short-acting (bolus)
Regular with onset of action 30 to 60 minutes
Injected 30 to 45 minutes before meal
Onset of action 30 to 60 minutes
(Basal) Background Insulin
Used to control glucose levels in between meals and overnight
Long-acting (basal)
Insulin glargine (Lantus) and detemir (Levemir)
Released steadily and continuously with no peak action
Administered once or twice a day
Do not mix with any other insulin or solution
Intermediate-acting insulin
NPH
Duration 12 to 18 hours
Peak 4 to 12 hours
Can mix with short- and rapid-acting insulins
Cloudy; must agitate to mix
Combination Insulin Therapy
Can mix short- or rapid-acting insulin with intermediate-acting insulin in same syringe
Provides mealtime and basal coverage in one injection
Commercially premixed or self-mix
Storage of insulin
Do not heat/freeze
In-use vials may be left at room temperature up to 4 weeks
Extra insulin should be refrigerated
Avoid exposure to direct sunlight, extreme heat or cold
Store prefilled syringes upright for 1 week if two insulin types; 30 days for one
Administration of insulin
Typically given by subcutaneous injection
Regular insulin may be given IV
Cannot be taken orally
Absorption is fastest from abdomen, followed by arm, thigh, and buttock
Abdomen is preferred site
Do not inject in site to be exercised- Can have altered peak times
Rotate injections within one particular site
Insulin pump- While doing assessment check for pump
Continuous subcutaneous infusion
Battery-operated device
Connected to a catheter inserted into subcutaneous tissue in abdominal wall
Program basal and bolus doses that can vary throughout the day
Potential for tight glucose control
Problems with insulin therapy
Hypoglycemia
Allergic reaction
Lipodystrophy- The SQ tissue gets atrophied from constant injections
Somogyi Effect
Somogyi effect- Will have high BS in the AM- Giving to much insulin causing BS to drop
Rebound effect in which an overdose of insulin causes hypoglycemia
Release of counterregulatory hormones causes rebound hyperglycemia
A bedtime snack, a reduction in the dose of insulin, or both
Dawn Phenomenon
Dawn phenomenon- Hyper glycemic- Check BS between 0200-0400
Morning hyperglycemia present on awakening
Due to release of counterregulatory hormones in predawn hours
Increase in insulin or an adjustment in administration time
Oral Agents
Work on three defects of type 2 diabetes
Insulin resistance
Decreased insulin production
Increased hepatic glucose production
Can be used in combination
Biguanides
Metformin (Glucophage)- Do not give somenof the oral ones. They interfere with contrast media
Reduce glucose production by liver
Enhance insulin sensitivity
Improve glucose transport
May cause weight loss
Used in prevention of type 2 diabetes
Withhold if contrast medium is used
Withhold if patient is undergoing surgery or radiologic procedure with contrast medium
Day or two before and at least 48 hours after
Monitor serum creatinine
Contraindications
Renal, liver, cardiac disease
Excessive alcohol intake
Sulfonylureas
↑ Insulin production from pancreas
Major side effect: hypoglycemia
Examples
Glipizide (Glucotrol)
Glyburide (Micronase, DiaBeta, Glynase)
Glimepiride (Amaryl)
Meglitinides
↑ Insulin production from pancreas
Rapid onset: ↓ hypoglycemia
Taken 30 minutes to just before each meal
Should not be taken if meal skipped
Examples
Repaglinide (Prandin)
Nateglinide (Starlix)
α-Glucosidase Inhibitors
“Starch blockers”
Slow down absorption of carbohydrate in small intestine
Take with first bite of each meal
Example
Acarbose (Precose)
Miglitol (Glyset)
Thiazolidinediones
- Most effective in those with insulin resistance
- Improve insulin sensitivity, transport, and utilization at target tissues
- Examples
–Pioglitazone (Actos)- Can cause myocardial infarction
–Rosiglitazone (Avandia)- Increase risk of blood cancer
•Rarely used because of adverse effects
Dipeptidyl Peptidase–4 (DDP-4) Inhibitor
Blocks inactivation of incretin hormones
↑ Insulin release
↓ Glucagon secretion
↓ Hepatic glucose production
Examples (gliptins)
Sitagliptin (Januvia)
Saxagliptin (Onglyza)
Linagliptin (Tradjenta)
Diabetes Nutritional Therapy
Counseling
Education
Ongoing monitoring
Interdisciplinary team with registered dietitian as lead
Diabetes Nutritional Therapy: Type 2 DM
ADA healthy food choices for improved metabolic control
Emphasis on achieving glucose, lipid, and blood pressure goals
Weight loss
Nutritionally adequate meal plan with ↓ fat and CHO
Spacing meals
Regular exercise
Carbohydrates
Minimum of 130 g/day
Fruits, vegetables, whole grains, legumes, low-fat milk
Monitor with CHO counting, exchanges, or experienced-based estimation
Glycemic index
Term used to describe rise in blood glucose levels after carbohydrate-containing food is consumed
High glycemic index foods increase glucose levels faster
http://www.glycemicindex.com
Fats
Limit saturated fats to less than 7% of total calories
Limit cholesterol to less than 200 mg/day
Two or more servings of fish per week to provide polyunsaturated fatty acids
Protein should make up 15% to 20% of total calories
Alcohol
Limit to moderate amount
Consume with food to reduce risk of nocturnal hypoglycemia
Fiber
Fiber-Recommendation: 25 to 30 g/day
•Carbohydrate counting
Serving size is 15 g of CHO
Typically 45 to 60 g per meal
Insulin dose based on number of CHOs consumed
Patient teaching essential
Diabetes Exercise
Start slowly after medical clearance
Monitor blood glucose
Glucose-lowering effect up to 48 hours after exercise
Exercise 1 hour after a meal
Snack to prevent hypoglycemia
Do not exercise if blood glucose level exceeds 300 mg/dL and if ketones are present in urine
Common manifestations of hypoglycemia
Shakiness
Palpitations
Nervousness
Diaphoresis
Anxiety
Hunger
Pallor
Altered mental functioning
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death
Hypoglycemic unawareness
lack of counterregulatory hormones
No warning signs/symptoms until glucose level critically low
Hypoglycemia Tx
Check blood glucose level
Treatment: rule of 15- 15 grams of carbs recheck in 15 minutes
In acute care settings
Fifty percent dextrose, 20 to 50 mL, IV push
Glucagon, 1 mg, IM or subcutaneously
Self-Monitoring of Blood Glucose
Patient teaching
How to use, calibrate
When to test
Before meals
Two hours after meals
When hypoglycemia is suspected
During illness- BS can increase
Before, during, and after exercise
Ambulatory and home care teaching
Overall goal is to enable patient or caregiver to reach an optimal level of independence
Use services of certified diabetes educator (CDE)
Establish individualized goals for teaching
Include family and caregivers
Assess patient’s ability to perform SMBG and insulin injection
Assess patient/caregiver knowledge and ability to manage diet, medication, and exercise therapy
Teach manifestations and how to treat hypoglycemia and hyperglycemia
Frequent oral care
Foot care- Check their feet daily, Don’t go barefoot, Cut their nails straight
Travel needs- Time change. Keep your watch to your regular time to keep your medications on track, Have someone with you. Know what your hypoglycemia symptoms are and carry snacks.
Chronic Complications Diabetic Retinopathy
Microvascular damage to retina
Most common cause of new cases of adult blindness
Nonproliferative: more common, early stage
Proliferative: more severe
•Nonproliferative
Partial occlusion of small blood vessels in retina causes microaneurysms
Proliferative
Involves retina and vitreous humor
New blood vessels formed (neovascularization): very fragile and bleed easily
Can cause retinal detachment
Diabetic retinopathy
Initially no changes in vision
Annual eye examinations with dilation to monitor
Maintain glycemic control and manage hypertension
Chronic Complications Diabetic Retinopathy Tx
Laser photocoagulation
Most common
Laser destroys ischemic areas of retina
Vitrectomy
Aspiration of blood, membrane, and fibers inside the eye
Drugs to block action of vascular endothelial growth factor (VEFG)
Chronic Complications Diabetic Nephropathy
Damage to small blood vessels that supply the glomeruli of the kidney
Leading cause of end-stage kidney disease
Risk factors
Hypertension
Genetics
Smoking
Chronic hyperglycemia
Annual screening
If albuminuria present, drugs to delay progression:
ACE inhibitors
Angiotensin II receptor antagonists
Control of hypertension and tight blood glucose control: imperative
Nerve damage due to metabolic derangements of diabetes
Of patients with diabetes, 60% to 70% have some degree of neuropathy
Reduced nerve conduction and demyelinization
Sensory or autonomic
Sensory neuropathy
Loss of protective sensation in lower extremities
Major risk for amputation- Do to poor foot care
Distal symmetric polyneuropathy
Most common form
Affects hands and/or feet bilaterally
Loss of sensation, abnormal sensations, pain, and paresthesias
Treatment for sensory neuropathy
Tight blood glucose control
Drug therapy
Topical creams
Tricyclic antidepressants
Selective serotonin and norepinephrine reuptake inhibitors
Antiseizure medications
Autonomic neuropathy
Sexual function
Erectile dysfunction
Decreased libido
Vaginal infections
Neurogenic bladder → urinary retention
Empty frequently, use Credé’s maneuver
Medications
Self-catheterization
