Diabetes Flashcards
Diabetes
A disease in which the body is unable to manufacture or utilize insulin thus resulting in a chronic state of hyperglycemia
Characterized by :
Disturbances of carbohydrate, lipid and protein metabolism
Beta-cell destruction leading to absolute insulin deficiency (Type 1)
OR
Insulin resistance with relative insulin deficiency (Type 2)
Secretory deficit with insulin resistance (Type 2)
Systemic organic changes as a result of vascular pathology
Facts about DM:
- Affects 7% of pop
- 7th leading cause of death in the US
- Leading cause of blindness, end-stage renal disease and amputations in the US
- 2-4x more likely to have heart disease
- **MI and CVA are leading cause of death for clients with DM
Pancreas: exocrine function
98% of pancreas is digestive enzymes
Pancreas: endocrine fumction
Islets of Langerhans…scattered through the organ most prominently found in the tail
Alpha, Beta, Delta
Secretion of hormones: Glucagon, Insulin and Somatostatin
Insulin
- A protein made up of amino acids
- Allows the glucose to move into the cells for energy
- Insulin reaches the liver first where it helps the liver produce and store glycogen and inhibits glycogen breakdown into glucose
- Increases protein and lipid synthesis
- Limits ketogeneisis (conversion of fats to acids) and gluconeogenesis (conversion of proteins to glucose)
- Keeps lipid levels in normal range and prevents glucose levels from being too high
Ketogenesis
conversion of fats to acids
Gluconeogenesis
conversion of protein to glucose
Lack of insulin
- Unable to store glucose
- Cells starve …fats break down for energy… ketones form
- Stored glucose dumps into bloodstream
- Glucose breaks down into CO2 +H2O
- Fluid and electrolyte imbalances
- Polyuria, polydipsia, polyphagia
Polyphagia
excessive hunger
Polydipsia
excessive thirst
Risk factors:
- Genetics
- Obesity > 20% IBW or BMI >25 kg/m2
- Body shape: apple v. pear
- Habitually inactive
- Ethnic group (AA, American Indian, Hispanic American, Asian American, Pacific Islander)
- HTN > 140/90
- HDL 250
- PMH Gestational diabetes or babies >9 pounds
- Polycystic ovary syndrome
- IFG or IGT on previous testing
Type 1 Diabetes
• Insulin dependent ◦ Absolute insulin deficiency ◦ Ketoacidosis (DKA) ◦ Usually younger than 30 y/o ◦ <10% of all DM
Type 2 Diabetes
• Non-insulin dependent ◦ Insulin resistance ◦ Abnormal secretion of insulin ◦ Impaired gluconeogenesis ◦ Obesity in 80% of clients ◦ 90% of DM
Treatment: Type 1
◦ Exogenous insulin
◦ Dietary control
Treatment: Type 2
◦ Lifestyle changes
Dietary control
Weight reduction
Exercise
◦ May require oral hypoglycemic therapy or exogenous insulin
– Insulin when oral hypoglycemic medications can no longer provide glycemic control
Diagnosis: health history
◦ Age ◦ Weight and weight changes ◦ Excessive hunger ◦ Excessive urination ◦ Excessive thirst ◦ Excessive fatigue ◦ Slow wound healing ◦ Infections ◦ Family hx DM
Diagnosis: blood glucose
◦ FBS > 126 (fasting = NPO x 8h)
◦ 2-hour plasma glucose > or = 200 mg/dL during an OGTT
◦ Symptoms of DM and random BG >200mg/dl
◦ The above 3 should be repeated to confirm Dx of DM
Diagnosis: HbA1C
◦ HbA1C > or = 6.5% (newly recognized as diagnostic criterion)
◦ Used to monitor glycemic control and predict risk for chronic complications
Target labs for diabetic patients:
- Blood Glucose
- Fasting: 90-130 (70-100 in non-diabetics)
- Bedtime: 100-140
- HbA1C: < or =7%
- Lipids
LDL: < 100 mg/ dL
HDL: >40 (men)
> 50 (women) ( with exercise and good fats)
Triglycerides: < 150 - Blood pressure: 130/80
Prevention of progression:
• Lifestyle changes Increase in physical activity Decrease in dietary fat Modification of food intake • Smoking cessation • Tx of HTN • Tx of hyperlipidemia • Tight control of blood glucose levels • Regular F/U with HCP or endocrinologist • Yearly vision testing Yearly urine microalbumin levels
Secondary diabetes
Pregnancy (Gestational diabetes) ◦ Weight gain, increased estrogen levels and placental hormones Pharmacological: ◦ Insulin antagonists ◦ Adrenal corticosteroids ◦ Contraceptives (po) ◦ Estrogen replacements ◦ Atypical antipsychotics Surgical removal of pancreas or pancreatitis Adrenal or pituitary gland disorders Viral infections ◦ CMV, rubella, mumps, adenovirus
Hyperglycemia: S/s
Hot, dry skin Dehydration Rapid, deep respirations; Kussmaul From alert to stuporous; coma N/V, cramps Tachycardia, orthostatic hypotension Positive ketonuria Notify HCP: BS >250 Cannot take food or fluids Ill more than 1-2 days Ketonuria lasts more than 24 hours
Sick Days:
Notify HCP of illness Monitor BG q4h Test urine for ketones Continue taking insulin or po antidiabetics Increase fluids, eat regular meals Get plenty of rest Treat symptoms as directed by HCP Know when to call HCP!
Acute Complications of DM:
1.Diabetic ketoacidosis (DKA) Lack of insulin Presence of ketones 2.Hyperglycemic-hyperosmolar state (HHS) Insulin deficiency Profound dehydration 3. hypoglycemia
DKA
Total or partial lack of insulin
Occurs with Type 1 diabetes
Most often starts with infection
Death – up to 10% of cases…even with appropriate treatment!
o Mortality highest in older adults with accompanying stroke, MI, vascular thrombosis, intestinal obstruction, or pneumonia
Increased renal and liver glucose production
Decreased use of glucose in tissues
Production of ketoacids – ketonemia and ketonuria – metabolic acidosis
Osmotic diuresis - dehydration and electrolyte loss
DKA: S/s
Sudden onset Polyuria, polydipsia, polyphagia Weight loss Vomiting, abdominal pain Dehydration, dry skin, weakness Altered mental status – total alertness to coma Shock Kussmaul respirations, fruity breath (from acetone exhaled)
DKA: lab findings
Glucose: >300 mg/dL Serum ketones: positive Serum pH: < 7.35 Serum HCO3: 20 mg/dL CrS: >1.5 mg/dL Urine ketones: positive
DKA: Monitor
o VS q 15mins til stable o Labs: hourly BGM, lytes o I/O: hourly outputs o IVF replacement Insulin drips o Neuro status Keep safe o Airway
DKA: managing fluids and electrolytes
- Restore volume - isotonic normal saline 1 - 2 L over hour ;
- replace total body fluid loss - 0.45 NS, when sugar < 250 : D 5 + 0.45 NS - to prevent hypoglycemia and cerebral edema
DKA: drug therapy
- Insulin: decrease sugar 75-150 mg/dL/hr - continuous IV insulin drip ( half life 4 min);
- Watch for hypokalemia ( fatigue, muscle weakness, shallow respiration, paraletic ileus, hypotension, wek pulse); Give K+
- Severe acidosis: bicarb (pH < 7)
HHS
Formerly known as hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
Acute hyperglycemic crisis that can result in coma or death from severe dehydration
End result of sustained osmotic diuresis
Renal insufficiency – extremely high BG levels
Kidneys capacity to reabsorb glucose is exceeded
Decreased kidney perfusion associated with hypovolemia
More common in older adults with Type 2
Difference between DKA and HHS
Both have hyperglycemia and dehydration. With HHS there are little or no ketones present; and glucose is much higher.
HHS: S/s
◦ Gradual onset ◦ May have seizures, myoclonic jerking, and reversible paralysis ◦ Serum glucose: >600 mg/dL ◦ Serum ketones: negative ◦ Serum pH: >7.4 ◦ Serum HCO3: >20 ◦ Urine ketones: negative
HHS: TX
Rehydrate: BS levels may drop 80-200 mg/dl with fluids alone
Caution with the elderly with hx cardiac a/o renal problems
Correct electrolytes
Hold insulin if K+ is less than 3.3
Na, Phosphorous and Mg++ replaced according to labs
Provide insulin to restore and maintain normal glucose
Hydration is key! Insulin is not always required once the client is re-hydrated
HHS: monitor
VS q 15 til stable Labs: hourly BGM, electrolytes I/O -hourly outputs IVF replacement Insulin drips Airway Neuro status Keep safe
Hypoglycemia
BG < 70 mg/dL Clinical criteria is used to categorize severity rather than BG levels Precipitating factors include: ◦ Too much oral med or insulin ◦ Increased activities ◦ Recent illness ◦ Wt loss ◦ Skipped or delayed meals ◦ Liver dysfunction ◦ ETOH without food
Hypoglycemia: S/s
Cool, clammy skin Profuse perspiration Anxiety, nervousness Irritability, mental confusion, seizures, coma Weakness Double vision, blurred vision Hunger Tachycardia, palpitations
Hypoglycemia: nursing considerations
All diabetics should be on hypoglycemia protocol while in hospital
Document all episodes
Notify MD for insulin/medication adjustment as needed
More likely to have another episode in next 24 hrs because glycogen stores in the liver have been depleted
Pts with chronic hyperglycemia may have s/s of hypo without going below a BG of 70mg/dl
Systemic effects of DM
25% of Medicare’s TOTAL budget is spent on treatment of diabetes and the chronic complications that go along with it
2 categories of chronic complications
◦ Macrovascular complications
◦ Microvascular complications
Macro-vascular changes
Refers to arteriosclerotic and atherosclerotic changes in moderate- to large-sized arteries and veins
Coronary artery disease, cerebral artery disease and peripheral artery disease fall into this category
Micro-vascular changes
Refer to disease of the small vessels
Nephropathy: damage to glomeruli
Retinopathy: damage to vessels of the retina
Neuropathy: damage to nervous system
CAD
◦ Most common complication of DM
◦ 2-3x greater risk than non-diabetics
◦ MI leading cause of death in diabetics
CVA
cerebra-vascular accident (stroke);
◦ Risk for stroke from vascular damage.
◦ Risk increased with HTN, hyperlipidemia, nephropathy, PVD and etoh/tobacco
PVD
◦ Poor blood flow to extremities
◦ 86,000 amputations/year and 85% of the time preceded by a foot ulcer
Targets for healthier heart
A1c < 6.5% Blood pressure < 200mg/dl HDL >40mg/dl for men; > 50 mg/dl for women LDL < 100 mg/dl Triglycerides < 150 mg/dl Smoking cessation Increase activity Weight loss
Diabetic Retinopathy
Leading cause of blindness in America Biggest fear of diabetics Related to duration of DM ◦ Type I - after 20 years close to 100% ◦ Type II - after 20 years > 60% Linked to FBG > 129 mg/dL Hyperglycemia and HTN increase the rate of retinopathy development in Type 1 Maintenance of near-normal BG levels reduces risk
Neuropathy
Common complication, often involves all parts of the body
Progressive deterioration of nerves, loss of nerve function
Results in pain and/or loss of sensation, muscle weakness
Peripheral neuropathy – numbness, tingling, burning sensation in hands and feet
Peripheral Neuropathy treatment:
◦ Normalization of blood sugars
◦ Medications like gabapentin (Neurontin
Autonomic Neuropathy treatment
◦ BG normalization
◦ Symptom relief with meds
◦ Smaller frequent meals, low fat and low fiber (gastroparesis)
◦ Hydration and elastic stockings for orthostatic BP
Goals for foot care:
1. Relieve pressure ◦ Proper foot wear ◦ Examination by HCP-deformities/nail care 2. Prevent ulcers ◦ Daily feet inspection ◦ Moisturizers (not between toes) 3. Prevent amputations ◦ Risk factor modification is essential!!!!!!!!!!
Foot care DO’s
◦ Wash feet daily in warm water ◦ Dry feet thoroughly ◦ Inspect daily for cuts, blisters, redness, calluses ◦ Exercise daily ◦ Custom made shoes ◦ See a podiatrist
Foot care DON’T
◦ Hot water ◦ Hot water bottles ◦ Heating pads ◦ Apply ice ◦ Soak feet ◦ Use OTC wart remedies ◦ Trim toenails ◦ Walk barefoot ◦ High impact aerobics ◦ Smoke
Nephropathy
Pathologic change in the kidney that reduces renal function and leads to kidney failure. Leading cause of end-stage kidney disease (ESKD) and kidney failure Diagnosed by laboratory tests Risk factors: ◦ 10-15 year history of DM ◦ Diabetic retinopathy ◦ Poor BG control ◦ Uncontrolled HTN ◦ Genetics
Nephropathy: treatment and prvention
Annual screening (including albumin level in urine)
BG control
BP control
Antihypertensive medications to protect the kidneys
Protein restriction
Avoid nephrotoxic drugs ( NSAIDS, pcn, dyes)
Avoid ETOH
Dental Disease
Higher risk for dental caries and gum disease due to increased glucose in saliva and damage to vessels of the gums
Dental exam every 6 months
DM: treatment
EDUCATE EDUCATE EDUCATE Prevention Diet Exercise Monitor BS, HbA1C, Lipids, BP Lifestyle modification Insulin and/or oral hypoglycemics
Principles of nutrition:
- Individualized diet plan:Meet with dietician
- Protein:15-20% of total daily calories (depending on renal function)
- Carbohydrates: 45-65% of total daily calories;Minimum intake of 130 g/day
- Fat and cholesterol: Saturated fatty intake < 7% of total daily calories;
- Dietary cholesterol < 200 mg/day
- Fiber (improves carbohydrate metabolism)
- ETOH (only with or after meal; in moderation)
- Diets: Exchange system based on 3 food groups; CHO counting; more flexible
Exercise
First see HCP Start slow and build Can cause hypoglycemia due to increased muscle glucose uptake and inhibited glucose release from the liver ◦ Up to 24 hours after exercise Benefits ◦ Better regulation of BG levels and lower insulin requirements ◦ Increased insulin sensitivity ◦ Decreased risk for CVD Don’t exercise if BG 250!!
Oral Hypoglycemics
- Sulfonylureas (oldest)
- Meglitinides
- Biguanides
- Alpha-glucosidase inhibitors
- Thiazolidinediones (TZDs)
Indications for oral hypoglycemics
They are used to lower blood sugar levels in patients when diet and exercise have failed.
The patient must have some pancreatic function left.
They can be used as a monotherapy or in conjunction with other oral hypoglycemics.
Sulfonylureas
Stimulate the pancreas to secrete more insulin
Usually well-tolerated and safe
Hypoglycemia possible
Weight gain
Peaks and valleys (snack?during peak time)
Many are only effective for a few years, then may stop working
Meglitinides
Action similar to sulfonylureas
Increase insulin secretion from the pancreas
repaglinide (Prandin)
nateglinide (Starlix)
Designed to increase meal-related insulin secretion
Rapidly absorbed
Short duration of action
Biguanides
Decrease liver production of glucose and improve insulin receptor sensitivity in tissues
Metformin does not produce hypoglycemia or weight gain;
Relatively low cost;
Few adverse effects: abdominal discomfort and diarrhea;
Recommended by ADA as initial tx for Type 2
Alpha-glucosidase Inhibitors
acarbose (Precose)
miglitol (Glyset)
- Reversibly inhibit the enzyme alpha-glucosidase in the small intestine
Result: delayed absorption of glucose and digestion of starches
◦ Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)
Thiazolidinediones (TZDs)
Decrease insulin resistance
Improves glucose control
◦ Increase glucose uptake and use in skeletal muscle
◦ Inhibit glucose and triglyceride production in the liver
pioglitazone (Actos)
rosiglitazone (Avandia)
Insulins:
Substitute for & same effects as endogenous insulin
Restores the diabetic patient’s ability to:
◦ Metabolize carbohydrates, fats, and proteins
◦ Store glucose in the liver
◦ Convert glycogen to fat stores
- Most now human-derived, using recombinant DNA technologies
Goal: tight glucose control by mimicking the pancreas’ normal insulin release pattern
- To reduce the incidence of long-term complications
Rapid -Acting Insulin
- Insulin aspart (Novolog) (0.25; 1-3; 3-5 hr)
- Insulin glulisine (Apidra)
- Human lispro inj. (Humalog)
Short -Acting Insulin
- Regular human insulin inj. (0.5; 2-4; 5-7 hr)
Intermediate - Acting Insulin
- NPH inj (1.5; 4-12; 16-24+ hr)
2. Lente
Long-Acting Insulin
- Ultralente
2. Insulin Glargine (2-4;none; 24)
Insulin : pharmacological therapy
Type I diabetics need insulin to survive
Type II diabetics may need insulin as time goes on
Insulin that is in use may be at room temperature for up to 28 days
Insulin that is not being used should be stored in the fridge
Discard insulin as per manufacturer recommendations
Use insulin syringe once and dispose of properly
Factors affecting absorption rate of insulin
The longer the duration of action, the more unpredictable is absorption
Larger dose – prolonged absorption
Increased blood flow from the injection site increases absorption
◦ Application of heat
◦ Massage of area
◦ Exercise of area
Scarring from repeated injections slow absorption rate
Injection depth of insulin
Injections should be made into SC tissue
◦ Most people grasp skinfold and inject at 90o
◦ Thin pt may need to inject at 45o to avoid IM
IM injection has faster absorption rate
Assess older patient’s ability to inject properly
Arrange for assistance when self-care not possible
Timing of injection
- Interval between pre-meal injection and eating is called “lag time”
- Lag time can be utilized to increase or decrease the absorption of insulin, therefore affecting the post-prandial BG level
Lipoatrophy
◦ The loss of fat tissue at site of repeated injections
◦ Caused by immune response to impurities in insulin
◦ Tx: injection of insulin at the edge of the atrophied area.
Lipohypertrophy
◦ Increased swelling of fat that occurs at site of repeated injections
◦ Decreased sensitivity, can become large and unsightly
◦ Tx: rotating the injection site among different body areas
Dawn phenomenon
◦ Morning hyperglycemia due to nighttime release of growth hormone causing BG elevation
◦ Occurs early: 5-6 a.m.
◦ Tx: provide more insulin for the overnight period
Somogyi phenomenon
◦ Morning hyperglycemia caused by the counterregulatory response to nighttime hypoglycemia
◦ Tx: ensure adequate dietary intake at bedtime and evaluate insulin dose and exercise program to prevent conditions that lead to hypoglycemia
Both are diagnosed by BGM during the night
Nursing care: Insulin
- BG monitoring
- Administration utilizing 5 rights and 2 identifiers
- Know onset, peak and duration of action
- Look at pt’s trends for 24 hr
- What is po status? (Lantus and Levamier have no peak and can be given)
- Plan ahead for procedures and surgery
- Know s/s of hyper/hypoglycemia
- Patient teaching in self-administration
- Site rotation
Lispro
Humalog - 0.5 -1.5 hr ( rapid - acting insulin)
Regular
Humulin R and Novolin R - 2-5 hr ( short-acting insulin)
NPH
Humulin N and Novolin N - 6-12 hr ( intermediate-acting insulin)
Glargine
Lantus - none ( long-acting insulin) never mixed .
FBG
fasting blood glucose < 100 ( > 126 )
OGTT
oral glucose tolerance testing ( 2 hr post) < 140 ( > 200 )
HbA1C
shows the average blood glucose levels during the previous 120 days - 4-6 % ( > 6.5 %)
Tolbutamide
Sulfonylurea agent; increase insulin secretion; take after meals; hypoglycemia.
Glipizide
Second generation sulfonylurea agent; increase insulin secretion; 30 min before meal; hypoglycemia; monitor for impaired renal function.
Metformin
Biguanide; (Glucophage); reduce hepatic glucose production; take with food; monitor renal and liver, cardiopulmonary function ; lactic acidosis; withhold for 48 hours before use of iodinated contrast materials.
Lactic acidosis
Lactic acid is produced when oxygen levels in the body drop.
Conditions that increase risk for lactic acidosis
Reduced renal function; liver impairment; respiratory insufficiency; severe infection; alcohol abuse.
S/s of lactic acidosis
Malaise, unusual muscle pain; respiratory and abdominal distress
Avandia
Thiazolidinedione (TZD); improves tissue sensitivity to insulin; Not for patients with moderate to severe liver impairment, jaundice ; may interfere with oral contraceptives ; monitor weight, assess for edema; continue therapy - response can take 2-3 month.
Pancreas secrets
40-50 units of insulin
