Test 2 Concept 6 Diabetes Lewis Ch 48, Giddens Ch 15

Hemoglobin A1C at time of diagnosis

- 50-80% of beta cells are no longer secreting insulin - Avg person has had diabetes for 6.5 years - For non-diabetic 5.7% - 6.5-7% for a diabetic is normal, can go over 10 but seriously uncontrolled at that point

Leading cause of

- Adult blindness - End stage renal disease - Nontraumatic lower limb amputations

Test

- Before meals - Two hours after first bite - Suspected hypoglycemia - Every 4 hours during illness - Before and after exercise

Risk hypoglycemia when exercising

- Carry fast-acting source of carbs in case of blood sugar drop - Frequent low glucoses, consult HCP about lowering meds

Insulin/glucose cycle

- Cells break down glucose to make energy - Liver and muscle cells store excess glucose as glycogen; anabolic (storage) hormone

Diabetes mellitus

- Chronic multisystem disease characterized by hyperglycemia related to abnormal insulin production, impaired insulin use, or both - 29.1mill people in US (8.1mil unaware, 86mil prediabetes) - Seventh leading cause of death

ADA guidelines for nutrition therapy

- Eat same food as non-diabetics: ratios of carbs:proteins, fats and alcohol - Normal lipid profile and blood pressure - Prevent or slow complications - Individual needs, personal/cultural preferences - Maintain pleasure of eating with healthy choices

Type II nutrition therapy

- Emphasis on achieving glucose, lipid and BP goals - Moderate weight loss (5-7%) improves insulin sensitivity - Effectiveness of therapy monitored by glucose, A1C, lipids and BP

Overall goals

- Engage in self care behaviors to actively manage diabetes - Few or no hyperglycemia/hypoglycemia emergencies - Maintain normal/near-normal blood glucose levels - Prevent risk for chronic complications - Adjust lifestyle to accommodate diabetes plan with minimal stress

Objective data

- Eyes: soft, sunken, cataracts - Integumentary: warm, dry, ulcers, loss of hair on toes - Respiratory: kussmaul respirations: breath smells sweet - Cardiovascular: hypotension, weak, rapid pulse - Gastrointestinal: dry mouth, vomiting, fruity breath - Neurologic: restlessness, altered reflexes, confusion, stupor, coma - Musculoskeletal: muscle wasting

A1C

- Glycosylated hemoglobin: reflects glucose levels over past 2-3 months - Glucose attaches to hemoglobin, higher the glucose levels-higher A1C - Used to diagnose, monitor response to therapy and screen prediabetics - Goal less than 6.5-7%

Gestational diabetes

- High risk: Obesity at time of pregnancy, advanced maternal age over 35, family history - 2-10% of US pregnancies - Increased risk for C section and perinatal/neonatal complications - Test week 24-28 and 6 weeks post partum - 63% chance of type II within 16 years if they have gestational

Nursing assessment

- History: viral infections, trauma, infection, stress, pregnancy, chronic pancreatitis, cushing syndrome, acromegaly - Meds: Insulin, OAs, corticosteroids, diuretics, phenytoin - Recent surgery/other treatment

ADA: 4 classes of diabetes

- I, II, gestational (usu after pregnancy disappears but is an indication for later on, usu big babies and also need to be tested), other

Implementation

- ID, monitor, teach patients at risk - Obesity: primary risk factor of type II

Genetic link

- Idiopathic diabetes: inherited - Latent autoimmune diabetes in adults (LADA) - slow, progressive type 1

Onset of Type I

- Islet cell autoantibodies are present for months-years before symptoms - Manifestations develop when pancreas can no longer produce insulin, then rapid onset with ketoacidosis - Sudden weight loss b/c cells can't get energy - Polydipsia: increased thirst: cells know starving and dehydrated - Polyuria: increased urination - Polyphagia: hungry, eating a lot, but still loosing weight - Requires exogenous insulin - Patient may have temporary (3-12 mo) remission after initial treatment

Nursing diagnosis

- Lack of knowledge - Hyper/hypoglycemia - Risk for injury: with neuropathy can't feel - Impaired peripheral neurovascular function

Alcohol

- Limit to moderate amount - Inhibits glucogenesis by liver: hypoglycemia - Eat carbs when drinking unless have sweetened mixers - Create trust for patients to honestly report intake

Acute illness/surgery

- May require different insulin treatments - Physical and emotional stress causes increased glucose - Stress --> more intense treatment to maintain glycemic goals - Glucose increase secondary

Interprofessional care

- Patient and caregiver teaching - Exercise: lowers blood glucose levels and increases insulin activity - Drug therapy: insulin, oral agents, noninsulin injectable agents - Self-monitoring of blood glucose - Type II: may not need medication if lifestyle changes happen

Pancreas type II

- Produces some endogenous insulin but either not enough or body does not use effectively - Different from Type I in which there is an absence of endogenous insulin

Theory of cause

- Single or combination of factors - Genetic, autoimmune, environmental

Culturally competent care

- Strong influence on dietary preferences and meal prep - High incidence of diabetes: Hispanic, Native American, Black, Asian, Pacific Islander

Patient teaching for prediabetes

- Undergo screening; glucose and A1C - Learn and manage risk factors - Monitor symptoms of diabetes - Maintain healthy weight, exercise, make healthy food choices

Subjective data

- Weight changes, thirst, hunger, nausea, - Elimination: constipation/diarrhea, frequent urination, bladder infections, nocturia - Muscle weakness, fatigue - Headache, blurred vision - Impotence, decreased libido, frequent vaginal infections - Depression, irritability, apathy

Critically ill target goal

140-180mg/dL, may get insulin if glucose consistently greater than 180mg/dL

Stable glucose

74-106mg/d

Exercise

ADA recommends 150min/week moderate-intensity aerobic activity. Resistance training 3xweek - Decrease insulin resistance - Weight loss - Reduce need for meds in type II - Glucose lowering effect lasts up to 48 hours

Autoimmune disorder

Body develops antibodies against insulin/pancreatic beta cells that produce insulin resulting in not enough insulin to survive - Predisposition and exposure to virus contribute to immune-related type I

Pathophysiology

Disorder of glucose metabolism related to absent/insufficient insulin/poor utilization of insulin

Diagnostic studies

Fructosamine, Islet cell autoantibody testing, Lipids, BUN, creatine, electrolytes, albuminuria/urine acetone

Major contributing factor

Heart disease and stroke (2-4x higher): may have hypertension and high cholesterol

Increased insulin

Inhibits glucogenesis, enhances fat deposition and increases protein synthesis

Fructosamine

Reflects glycemia in previous 1 to 3 weeks, May show change before A1C Used for hemoglobinopathies or short-term measurement of glucose levels

Personal hygiene

Regular oral, dental care, bathing, foot care, treat/monitor wounds

Decreased inslulin

Release glucose from liver, protein from muscle and fat from adipose tissue

Type II characteristics

adult-onset/non-insulin dependent - Most prevalent 90-95% - Gradual onset - Risk factors: overweight or obese, advanced age, family history - Different ethnicities have different likelihoods - Hyperglycemia without detection for many years - Often discovered with routine glucose testing or hemoglobin A1C

Insulin on drip

can only give regular; rapid can have increased risk for tumor formation

Greater than 240mg/dL

check urine for ketones every 3-4 hours 2 hours greater than 300mg/dL: report to HCP

Insulin

hormone produced by beta cells in islets of Langerhans - Released continuously into bloodstream in small increments with larger amounts released after food - Promotes glucose transport from blood to cell to give energy - Daily secretion by adult: 40-50 U - spike after meals b/c insulin increases to cover the sugar: must time insulin with the spikes

Prediabetes

increased risk for developing Type II - Impaired glucose tolerance (IGT): 140-199mg/dL - Impaired fasting glucose (IFG): 100-125mg/dL - Usu asymptomatic warning sign for lifestyle changes but long term damage already occurring

Nutritional therapy

individualized plan for diabetic and prediabetic patients include counseling, education, ongoing monitoring, considers behavioral, cognitive, socioeconomic, cultural, religious backgrounds and preferences

Normal

insulin binds to insulin receptors and triggers opening of glucose transporters in fat and muscle cells, allowing glucose removal from bloodstream

Type I

insulin not produced by beta cells in pancreas so glucose is not removed, cells do not get energy, blood has excess of sugar, absolutely must be on insulin

Type I characteristics

juvenile-onset or insulin-dependent - 5-10% of all people with diabetes - Generally under the age of 40: can occur at any age - Not as common as type II - Not sure of cause, autoimmune or genetic maybe

Medical ID and travel

medic alert or ID card for diabetes

Type II

produce some insulin, but not enough. OR signal is not working, does not open channel for glucose and still symptoms of hyperglycemia.

Interprofessional team

registered dietitian with expertise in diabetes management/ nurses, CDEs, CNS social worker, HCPs

Type II symptoms

same as type I but also - Recurrent uti - Recurrent vaginal yeast or candida infection - Prolonged wound healing - Visual problems

Ketoacidosis

spilling ketones in urine, breaking down muscles b/c cells have nothing else to sustain energy