TLO 2.3 Nutrition, Fluid, Diabetes Flashcards
What is diabetes mellitus
A disease in which the body doesn’t produce or properly use insulin, leading to hyperglycemia
What is type 1?
Pancreas makes little or no insulin
Destruction of beta cells leading to decline in and ultimate lack of insulin secretions
Leading to hyperglycemia, lipolysis and protein catabolism
What is type 2?
Genetic factor. Onset of obesity and sedentary lifestyle. Pancreas does produce some insulin but is usually too little or ineffective. Leading to inappropriate glucose production by the liver.
The three “P’s” of diabetes (hyperglycemia) assessment?
Polyuria= excess urination Polydipsia= excess thirst Polyphagia= excess hunger
What to look for in type 1?
Extreme thirst High levels of ketones in urine Lack of or increased appetite Drowsiness, lethargy Fruity odor of breath High glucose levels Rapid, hard breathing, Kussmaul respirations Eventual stupor to unconsciousness
What to look for in type 2?
Possible no symptoms Frequent urination Excessive thirst Fatigue Sores that slow heal Tingling/numbness in hands Dehydration Weight loss Extreme hunger Sudden vision changes
Risk factors
Immediate family member with diabetes Obesity Ethic group Gestational diabetic Hypertension Hyperlipidemia Previous testing A1C >6
Diagnostic testing?
A1C (3 month average, >7)
Fasting plasma glucose level >126 (hold anti-diabetic meds until blood drawn)
Two hour plasma glucose level
Random plasma glucose level 200 or greater
Presence of serum and urine ketones
Type 1 nursing interventions
Physical assessment Admin insulin Diet and nutrition education Education regarding physical exercise (sick day rules) Education of hypoglycemia or hyperglycemia Blood glucose and ketone monitoring Assessment of lab values Psychosocial support
Glucose lab values Toddler/preschool before meals? bedtime? A1C?
Toddler/preschooler
Before meals: 100-180
Bedtime: 110-200
A1C: <8.5
Glucose lab values School age before meals? bedtime? A1C?
School age
Before meals: 90-180
Bedtime: 100-180
A1C: <8`
Glucose lab values Adolescents before meals? bedtime? A1C?
Adolescents
Before meals: 90-130
Bedtime: 90-150
A1C: <7.5
Oral glucose tolerance test A, process
Fasting blood glucose level is drawn at the start of the test
Pt instructed to consume a specific amount of glucose
Blood glucose level drawn every 30 min for 2 hours
Pt needs to be assessed for hypoglycemia throughout procedure
Pt instructed to consume a balanced diet 3 days prior
Pt fast 10-12 hour prior to testing
Sick day rules
M, D, C, B, H, F
Monitor blood levels frequently Do not stop insulin Check urine for ketones Be careful with OTC Have a game plan Force fluids
Which insulin can be administered IV?
Regular
Preferred injection sites?
Posterior upper arm Legs/thigh (best absorption for children) Buttocks Abdomen (best absorption for adults) **SUBQ **Rotate sites
Adult fasting blood sugar lab value?
Adult
70-120 mg/dL
Teaching for diabetic patients
Pathophysiology Diet Exercise Medication Lab tests and glucose monitoring
Lab values that are monitored for Type 1 and why?
Magnesium
Phosphorus
Potassium
**Insulin can decrease these serum levels
Hyperglycemia s/s, glucose level, what to do?
Hyperglycemia (SLOW):
Elevated blood glucose >170
Causes excessive carbohydrate intake, inadequate insulin amounts, increased stress, infection
S/S: increased thirst/urination, fatigue, weight loss, blurred vision, hunger
What to do:
Notify provider, insulin, exercise, increased oral fluids, need sick day plan
Type 1 info/manifestations?
Age: Any age including infants
Predisposing factors: Genetic/environmental
Symptoms: 3 “P’s”, weight loss
Insulin therapy
Chronic complications: retinopathy, nephropathy, neuropathy, cardiovascular disease
Ketones: DKA, young children and adolescents
Type 2 info/manifestations?
Body becomes resistant to insulin production from pancreas
Middle age/older adult
Hereditary/lifestyle/obesity
Symptoms: children usually don’t have symptoms but diagnosed at wellness check up
Therapy: meds, diet, activity
Chronic complications: foot ulcers, heart/renal disease, PVD, retinopathy, nephropathy, neuropathy
Ketoacidosis
Hyperosmolar hyperglycemic syndrome (HHS)
Oral antidiabetic agents
Sulfonylureas (first and second gen) are used to treat mild, non-ketonic type 2 in pt who are not obese
Associated with weight gain
Usually held during hospitalization
Meglitinides stimulate release of insulin from islet cells
Biguanide (Glucophage) needs to be held before and 48 hours after iodinated contrast due to risk of renal failure
Alpha-glucosidase inhibitors
Thiazolidinediones
Combination therapy
Oral antidiabetic agents
What do you need to know to administer these medications?
Used to treat type 2
Medications lower blood sugar by stimulating or increasing insulin secretions, preventing breakdown of glycogen to glucose by the liver and increasing peripheral uptake of glucose by making cells less resistant to insulin
Some hypoglycemic agents keep blood sugar low by blocking absorption of carbohydrates in the intestines
5 main components of diabetes management include:
Education
Pharmacologic therapy
Monitoring
Exercise: encourage daily exercise; additional food intake half hour before activity and then every 45 min to 1 hr throughout
Nutrition therapy: teach glycemic index of food, appropriate snacks, sugar substitute with moderation
How may this disease effect development?
How does the age of the child affect your approach?
TODDLER-PRESCHOOLER
Toddler- preschooler:
Chooses and cleans finger, not yet able to understand the need for insulin, helps choose foods
Preschooler: Teach about disease and food choices on child’s cognitive level
How may this disease effect development?
How does the age of the child affect your approach?
SCHOOL AGE
School age
Performs finger stick, chooses injection site, pushes insulin syringe after needle is inserted by parent or give own injection
Teach self monitoring of blood glucose, urine testing and insulin injections
How may this disease effect development?
How does the age of the child affect your approach?
EARLY ADOLESCENT
Early adolescent
Draws up insulin with supervision, performs insulin injection, begins to manage insulin pump and carb counting. adds extras snack for increased activity
Explore needs for conformity with peers and nonadherence with medical regimen, increase self care, increase motivation with day off or occasional dietary treat
How may this disease effect development?
How does the age of the child affect your approach?
MIDDLE-LATE ADOLESCENT
Middle-late adolescent
Draws up and injects insulin. Recognizes when to test for ketones in urine and initiates treatment for ketones (fluid)
Hypoglycemia, s/s, level, what to do?
Hypoglycemia (RAPID):
Blood glucose level <60
Occurs as result of too much insulin, not enough food or excessive activity
S/S: Trembling, sweating, tachy, pallor, clammy skin irritability, drunken behavior, decreased LOC
What to do: 15G of carbohydrate, administer glucose, give snack, unconscious squeeze glucose paste or frosting onto gums and retest glucose level in 15 min, may admin glucagon (SQ or IM) or IV dextrose if patient unconscious or seizure activity
Diabetic Ketoacidosis what it is?
Leads to hyperglycemia, ketones in blood, metabolic acidosis.
Causes in younger diabetic is insulin resistance, stress response to infection
Adolescent: most common cause is one or more missed insulin injections. Usually need intensive care unit admit for hourly glucose monitoring, fluid and electrolyte monitoring (K+, Mg++, Phos) with IV fluids replacement and continuous IV insulin
Hypoglycemia T.I.R.E.D.
T: tremors and tachy I: irritability R: restless E: excessive hunger D: diaphoresis and depression **cold and clammy means you need candy **hot and dry means your sugar is high
Diabetic Ketoacidosis manifestations?
Glucose of >200 Serum bicarbonate of <15 Thirst Warm dry skin Dry mucous membranes Rapid weak pulse Hypotension Nausea/vomiting Lethargy Ketone breath Abdominal pain Kussmaul respirations Coma
Causes of morning hyperglycemia: two types
Somogyi effect
Dawn phenomenon
***What is Somogyi effect and treatment?
Normal or elevated blood glucose at bedtime, a normal decrease at 2-3am to hypoglycemic levels and a subsequent increase caused by the production of counter regulatory hormones
Nocturnal hypoglycemia followed by rebound hyperglycemia
Treatment: decrease evening dose intermediate acting insulin or increase bedtime snack
***What is Dawn phenomenon and treatment?
Relatively normal blood glucose until 3am, when the level begins to rise (hyperglycemic)
Phenomenon is thought to result from nocturnal surges in growth hormones secretions, which create a need for insulin in the early morning hours in patient with type 1
Treatment: change time of injection of evening intermediate acting insulin from dinner time to bedtime
Pathophysiology of type 1?
Type 1 diabetes is due to pancreatic islet B cell destruction predominantly by an autoimmune process, and these persons are prone to ketoacidosis
Pathophysiology of type 2?
Type 2 diabetes is the more prevalent form and results from insulin resistance with a defect in compensatory insulin secretion
Hyperosmolar hyperglycemic syndrome (HHS)?
Causes decrease insulin, older age (>60 year)
Less common than DKA
Can occur in type 1 or 2 but more common in type 2
Serious life threatening complication
Blood glucose >600
No Kussmaul respirations
Ketone are absent or minimal
Onset is slow, over several days
Precipitating events; physiologic stress, infection, surgery, CVA, MI
Treatment similar to DKA, correct fluid and electrolyte imbalances, insulin drip until blood glucose levels reach 250 because ketosis is not prevent there is not need to continue insulin until glucose 250
Referral needs
Dietician Endocrinologist (peds) Diabetes education Ophthalmology Podiatry
