Metabolism

Pharmacologic: diabetes in children (T2D)

Insulin -most oral medications for type 2 are only approved for children over 18 Usually only used if diet and exercise is not working or if HgA1c is consistently high Daily insulin dosage depends on age, weight, stage of puberty, duration/phase of diabetes, state of injection sites, nutritional intake/distribution, exercise patterns, daily routine, results of glucose monitoring, comorbid illness

Pharmacological: T1D

Insulin dependent -monitor blood glucose (type 1 MUST monitor their condition daily by testing their blood glucose) Insulin -Individuals with type 1 require administration of insulin lifelong -to lower glucose Check children blood sugar before meals and bed T2D will fluctuate because they still release insulin

The nurse is caring for a client with diabetes mellitus. What is the primary fluid shift that occurs with this condition?

Intracellular to intravascular because of hyperosmolarity The osmotic effect of hyperglycemia pulls fluid from the intracellular and interstitial compartments, resulting in dehydration. Hyperglycemia pulls fluid from the interstitial to the intravascular compartment, eventually spilling into the urine. Interstitial fluid is part of the extracellular compartment; the osmotic pull of glucose exceeds other osmotic forces. An increase in hydrostatic pressure results in an intravascular to interstitial shift.

Common signs of T1D

Polydipsia (excessive thirst) -due to the cells being dehydrated polyuria (excessive urination) -body is trying to compensate, it filters to the kidney and spills out into the urine polyphasia (excessive hunger) -they are not getting enough energy, cells are starving and will make you hungry

Complications: DKA

coma or death (depression of CNS from accumulation of ketones resulting in acidosis)

Fasting blood glucose

ordered if patient is experiencing symptoms of hypoglycemia or hyperglycemia

Urine glucose and ketones level

presence of glucose in the urine indicates hyperglycemia; when blood glucose exceeds 180 mg/dL glucose is not reabsorbed by the kidney and spills over into the urine Ketonuria (presence of ketones in the urine) occurs with the breakdown of fats and is an indicator of DKA or malnutrition ketones not as accurate

Manifestations: DKA

slow onset (4-10) result from severe dehydration and acidosis Irregular heartbeat/ increased pulse hyperkalemia hyponatremia (fluid being pushed out and sodium follows) Vomiting Stomach pain Rapid breathing Sleepiness Dry mouth Flushed face Fruity breath

How does the body get rid of extra floating sugar in T1D?

the body tries to breathe it off or it will go to the kidneys and spill into the urine (glycosuria) showing you have too much sugar in your blood polyuria due to body trying to get rid of all the sugar causing more dehydration Body starts metabolizing self (breaking down fat and protein) in which it develops ketones trying to keep cell function -increased ketones leads to metabolic acidosis -turns into DKA when ketones go into the bloodstream (metabolic acidosis -DKA= our body tried to breathe it off through respiration (kursimals)

Serum electrolyte

levels are measured in patients who have DKA or HHS (specific to T2D) to determine imbalances

Treatment for diabetic ketoacidosis

1. Metabolic Panel (first thing you do when someone presents with DKA) 2. Fluid replacement -initially 1L of NS over 1 hour -Hydrate with bolus of NS -Dilute back to normal -Administer NS, after 2-3 hours (or when blood pressure is returning to normal), administer 1/2 NS then when BG reaches 250, dextrose is added to prevent rapid decreases; hypoglycemia could result 3. Ensure potassium level of 3.3 mEq/L before initial therapy 4. Insulin via IV infusion (initially) -Regular insulin - mild ketosis (SubQ) Average stay is 4-6 days in hospital Hypovolemic- we will always use NS unless they have sodium level 150-200 (hypernatermia then use half normal saline) Admission: -BG level greater than 250 mg/dL -decreasing pH -ketones in the urine If pt is alert and conscious, fluids may be replaced orally If vomiting, LOC and acidosis = IV fluid replacement Electrolyte imbalances: -Priority K depleted body stores of potassium (decreases during treatment) -rehydration = body loses potassium from increased urinary output, acidosis, catabolic state and vomiting and diarrhea -potassium replacement to prevent cardiac dysrhythmias and hypokalemia HI-E

Type 1 collaboration (maintaining BG)

Closely controlled blood glucose -reduces risk of complications by 60% Focus of treatment: maintain blood glucose at nearly normal levels through- medication dietary, and exersice

normal fasting blood glucose

70-110 mg/dL

Diabetic ketoacidosis

Acute hyperglycemia complication (T1D) Most common complication of type 1 diabetes and is usually how diagnosis is made Potentially fatal Increased glucagon levels then lead to DKA May also occur when energy requirements increase (exercise) or "stressful" situations (infection or illness

Somogyi phenomenon

Acute hyperglycemic complication (T1D) hypoglycemia during the night with a rebound morning rise in BG to hyperglycemic levels causes insulin resistance for 12-48 hours

Dawn phenomenon

Acute hyperglycemic complication (both types) rise in BG between 4am-8am

Maintain safety (T1D)

Assess for presence of contributing or causative factors Reduce environmental hazards Monitor for and teach client, family -DKA in client with type 1 DM -HHS in client with type 2 DM -Signs, symptoms, treatment hypoglycemia Recommend wearing medical alert jewelry

Manifestations: Hypoglycemia

Blood glucose less than 50 mg/dL Coma, seizures, or altered behavior anxious or restless sweaty confused blurred or double vision shaky Irritable and hungry pale moist, cool skin

Managing complications: T1D in children

Celiac disease -immune mediated disorder characterized by the inability to hydrolyze peptides contained in gluten, occurs with increased frequency in individuals with T1D Thyroid disease -hypothyroidism Eating disorders -hyperglycemia present -> calories are lost and weight loss Hypoglycemia -higher risk than adults When you have one autoimmune disease you will usually have another Ever child needs a glucagon pen in their bag when they have diabetes and keep a log of their blood sugars We want to see their baseline and trends

Diagnostic test: T1D in children

Confirming presence of diabetes - Hemoglobin (A1C) level of 6.5% or higher -Random blood plasma glucose level of 200 mg/dL or higher (or fasting plasma glucose of 126 gm/dL or higher) Glucose monitoring -children require more frequent monitoring -different targets due to erratic oral intake activity presence or absence of immune markers ( C peptide levels/T2D) along with careful family history and evaluation of presenting symptoms

Pharmacologic: diabetes in children (T1D)

Daily insulin dosage depends on age, weight, stage of puberty, duration/phase of diabetes, state of injection sites, nutritional intake/distribution, exercise patterns, daily routine, results of glucose monitoring, comorbid illness Lower amounts of insulin given because we want to maintain and we do not know where they are at with their levels

Interventions: T1D in children

Education should be a priority and initiated as soon as possible Always assess child's developmental stage and take into consideration when making interventions Always assess barriers on implementations and work around them Be creative Be resourceful Involve Child Life

Diagnostic test: diabetes management monitoring

Fasting blood glucose Hemoglobin A1C Urine Serum Cholesterol and triglycerides Serum electrolytes

Risk factors: T1D

Genetics Populations (African Americans, Hispanics, American Indians) Family History Environmental factors

Preoperative screening: diabetes

Glucose monitoring Insulin dosing individualized -Client (type 1 or 2 DM) with pre-op glucose -Scheduled procedure early - Postoperative care (regular glucose monitoring) If NPO, short-acting insulin should not be given without IV glucose IV infusion of glucose, insulin, and added potassium is appropriate for hyperglycemia pt

Explain the process of T1D

If the body cannot push the sugar into the cells, the cells start to shrink and die off so the body compensates but taking energy (breaking down) fat and proteins you get ketones, so you have too many ketones in the blood we become acidotic, your sugar acts as an osmotic diuretic so you urine it out, the ketones are also filtered out the kidneys with the sugar from the bloodstream in which you become dehydrated from the polyuria Can be life threatening- we are in an acidic state and it causes massive dehydration

Maintain Sexual Health (T1D)

In both men and women Include sexual history Provide information about actual, potential effects Provide counseling Referrals as appropriate

Exercise: T1D

Regular exercise improves fitness, emotional state (it is important to assess what types of exercise the client enjoys to maintain compliance) -Weight control -Improved work capacity -decreases blood glucose and maintains homeostasis in the body Avoid exercise in extremes of hot, cold Time in relation to meals, injections Always teach to take glucose levels before exercise to prevent hypoglycemic episode. Levels should be above 100 mg/ml. If they are not before exercise they should ingest a carbohydrate. Monitor glucose before exercising -level should always be above 100 before they start exercising - have them eat carbs if not

Pathophysiology: T1D

Result of the destruction of beta cells of the islets of Langerhans in the pancreas- the only cells in the body that make insulin. When beta cells are destroyed, little or no insulin is produced Can be considered autoimmune, idiopathic or immune mediated Begins with insulinitis (chronic inflammatory process that occurs in response to autoimmune destruction of the islet cells. -This process slowly destroys beta cell production of insulin occurring with the onset of hyperglycemia when 90% of beta cell function is lost Insulin dependent diabetes Sometimes may present as DKA (diabetes ketoacidosis)

How in insulin given

Sub Q, insulin pump Vials and pens Biggest med errors- they can mix up the syringes (1mL instead of insulin) Insulin pump- you do not touch it as often but higher risk for infection since you do not change it as often; it regulates your insulin and checks blood glucose -regular or rapid acting -hold a small pump of insulin connected subQ needle through tubing -changed every 3 days -allow more normal regulation of blood glucose and lifestyle flexibility

Three levels of client teaching

Survival skills Home management Improving lifestyle, educating clients

Clinical Manifestations: T2D children

Symptoms may be less acute than those of type 1 DM Acanthosis nigricans (brown thing around neck) Obesity

Serum Cholesterol and triglycerides

indicates atherosclerosis and an increased risk of cardiovascular impairments Treatment goal- lower low-density lipoprotein (LDL) cholesterol to less than 100 mg/dL, raise high-density lipoprotein (HDL) cholesterol to more than 40-50 mg/dL and lower triglycerides to less than 150 mg/dL

Nonpharmacologic: T1D in children

infants and toddler: -frequent small meals may promote glycemic control Schoolchildren: -focus on adapting the diabetes regimen to fit the active life of the school age child. Give advice regarding carbohydrate intake to prevent hypoglycemia and how to adjust insulin and intake when sports activities are involved Adolescents: -weight monitoring is recommended for early recognition of both weight loss and inappropriate weight gain, which may be associated with insulin omission for weight control or may indicative of an eating disorder

Pathophysiology: DKA

insulin deficit causes fat stores to break down; the result is continued hyperglycemia and mobilization of fatty acids with a subsequent ketosis Develops when there is an absolute deficiency of insulin and an increase in the insulin counterregulatory hormone Glucose production of the liver increase peripheral glucose use decreases fat mobilization increases ketogenesis (ketone formation) is stimulated loss of bicarbonate; occurs when ketone is formed causing metabolic acidosis

What happens when the body does not make insulin in T1D?

too much sugar without insulin available results in sugar not being able to be pushed into the cells, (hypotonic) fluid is pulled from the cells causing them to shrink and die causing us to become dehydrated -more sugar in bloodstream and no insulin= no energy for cells because insulin pushes sugar -fluid pulled because no energy in the cell -sugar will continue to increase in which it stays in the bloodstream -no energy in the cell, body will breakdown fat Summary: Since the body in type 1 does not make insulin, there is none circulating to lower blood sugar, this causes a spike in the blood causing it to be hypotonc

Long acting (onset, peak, duration)

Onset: 2 hours (slide says 6-8 hours) Peak: no peak Duration: 24 hours purpose is to stabilize levels, given at bedtime to treat both diabetes, not recommended in pregnancy Types- Lantus (Glargine) (not mixed or used in pumps), Levemir (Detemir)

Short acting (onset, peak, duration)

Onset: 30-60 minutes Peak: 2-3 hours Duration: 4-6 hours Clear in appearance, only one that can be give IV, used to treat DKA, initiate tx for newly diagnosed T1D, provide better glucose control with intermediate Types- Novolin R, Humulin R (Regular)

Treatment begins with (T2D)

-weight loss -increased activity (exercise)

Diagnostic test: T2D

Overweight or obese (BMI greater than 25) who have one or more risk factors for T2D Measurement of FPG, a glycated hemoglobin (A1C) and a 2-hour PG during an OGTT (due to inconvenience the OGTT is not commonly used except in pregnant women)

Pathophysiology: T2D

A progressive condition caused by the inability of cells to respond to insulin. Insulin is not made as abundant by the beta cells. It was once known as insulin resistant diabetes. The insulin resistance overpass the ability of the body to produce enough insulin to meet the needs of the body. However, there is still enough to break down fats adequately. It is often related to as non-ketotic. Insulinitis Insulin resistance because it cannot attach to the sugar but some can push into the cell non ketotic because the cells are not starving highest risk for comorbidities in the end Usually do not have enough insulin or it is not working good enough to maintain blood sugar Are generally overweight Can't produce enough insulin to keep up with the glucose load Not as abrupt as Type 1 (occurs over time) Usually found by accident or during general physicals or if wounds will not heal Can occur at any age Inactivity

Promote healthy behavior (T1D)

Use, teach meticulous hand washing Monitor for manifestations of infection Discuss importance of skin care Teach dental health measures Teach women symptoms, preventive measures for Candida albicans

Onset: T1D

Usually diagnosed as a child and abruptly

Complications involving the feet

Chronic complication (T1D) Result of angiopathy, neuropathy, infection vascular changes usually bilateral diabetic neuropathy produces multiple problems Most common trauma -cracks, fissures from dry skin -blisters, pressure -ingrown toenails Begins as superficial ulcer -extends deeper Good resource- podiatrist (refer) Diabetics have decreased healing

Promote effective coping (T1D)

Client faced with lifelong changes Assess client's psychosocial resources Explore with client, family the effects -Treatment, occupation, energy levels, relationships Teach constructive problem solving Provide information about support groups, resources

HHS treatment

Correct fluid, electrolyte imbalances Lower blood glucose levels with insulin NS- we want to dilute blood back down Correct shock with adequate IV fluids If a patient is comatose, institute NG suction to prevent aspiration Maintain fluid volume with IV isotonic or colloid solutions, administering potassium IV to replace losses Administer insulin to reduce BG usually until levels reach 250mg/dL

After reviewing the 24-hour urine collection reports of a client with kidney dysfunction, the nurse suspects diabetes mellitus. Which finding supports this suspicion?

Creatinine level: 40 mg/kg/24 hr Blood urea nitrogen (BUN) and serum creatinine levels are increased in clients with kidney dysfunction. This results in nausea, vomiting, increased fatigue, muscle cramps, and anemia, resulting in decreased breakdown of insulin. The normal range of creatinine lies between 14 and 26 mg/kg/24 hr. Therefore a creatinine level of 40 mg/kg/24 hr indicates diabetes mellitus. A calcium level of 500 mg/24 hr indicates hyperparathyroidism, sarcoidosis, calcium kidney stones, and hypercalcemia. A sodium level of 300 mEq/24 hr indicates hypokalemia and acute tubular necrosis. A urea nitrogen level of 30 g/24 hr indicates trauma, sepsis, or infection.

Rapid acting insulin (onset, peak, duration)

Onset: 15-30 minutes Peak: 1-1 1/2 hours Duration: 3-4 hours Have to have food present at site before giving insulin or they will crash Types- Humalog (lispro), novolog (aspart), apidira (glulisine)

Risk factors: T2D

Diabetes in parents or siblings Obesity Physical inactivity Race/ethnicity History of gestational diabetes Polycystic ovary syndrome Hypertension Metabolic syndrome More prevalent in African Americans, American Indian, and Hispanic populations and more prevalent in men

Chronic complications: T1D

Diabetic nephropathy -disease of the kidneys characterized by the presence of albumin in the urine, hypertension, edema and progressive renal insufficiency -thickening of basement membrane of glomeruli -impairs renal function -hypertension accelerates progression -single stage that causes end stage diabetes Diabetic neuropathy -disorders of the peripheral nerves and the autonomic nervous system Diabetic retionpathy -three stages to changes in retina (S1: nonproliferative, S2: preproliferative, S3: proliferative- hemorrhage and retinal detachment where blindness comes from) Coronary artery disease -MI -Macrocirulation changes (causes neuropathy) -microcirculation changes Hypertension -BP greater than 140/90 Stroke (cerebrovascular accident) - (T2D) Peripheral Vascular disease -(T2D) -peripheral neuropathies (distal paresthesias) -Visceral neuropathies (sweating disfunction, abnormal pupillary function, cardiovascular dysfunction, GI dysfunction, genitourinary dysfunction) Alterations in mood Increased susceptibility to infection -vascular, neurological impairments -nephrosclerosis Periodontal disease

Sick day management: T1D

Guidelines -Monitor blood glucose at least 4 times a day -Test urine for ketone (becoming acidic) if BG is greater than 240 mg/dL -Continue normal insulin/hypoglycemic dose -Sip 8-12 oz fluid each hour -Substitute easily digested liquids (it will go straight into the blood) -Call healthcare provider

Diagnostic test: T1D

HbA1c greater than or equal to 6.5% Symptoms of diabetes plus casual plasma glucose concentration greater than 200 mg/dL (casual- any time of the day without regard to time since last meal) Fasting plasma glucose greater than 126 mg/dL (fasting- no caloric intake for 8 hours) 2 hour PG more than 200 mg/dL during an oral glucose tolerance test. Prediabetes - Blood sugar between 100-126 mg/dL -At increased risk of developing diabetes ADA- have to have at least 3 out of the 4

Combination insulin

Humalog 50/50 shor and intermediate- mixtures could be resistance

Complications: T2D

Hyperglycemia -Hyperosmolar hyperglycemic state Occurs in individuals with type 2 DM Plasma osmolarity ≥ 340 mOsm/L Blood glucose levels > 600 mg/dL Serious, life-threatening (higher than DKA) Precipitating factors- infection, therapeutic agent and procedures, acute illness, and chronic illness Slow onset Results in severe dehydration Hypovolemic shock high glucose Glucose and sodium accumulate in the blood and increase serum osmolarity Same as T1D

Manifestations: T1D in children

Hyperglycemia -increased thirst, hunger, urination -fatigue -blurred vision -irregular heartbeat (electrolyte imbalance) -weight loss

Intermediate acting (onset, peak, duration)

Onset: 2 hours Peak: 6-8 hours Duration: 12-16 hours cloudy appearance due to protamine and zinc Types- Novolin N, Humulin N (NPH)

Clinical Manifestations: T1D

Hyperglycemia -normal BG: 70-110 -prediabetes before 110 -results from the accumulation of glucose molecules in the circulating blood -causes hyperosmolality drawing water from the intracellular spaces into the general circulation Classic 3Ps -polyuria -polydipsia -polyphagia (side effects: weight loss, ketosis, ketoacidosis) Ketosis (accumulation of ketone bodies produced during oxidation of fatty acids) Recent weight loss, malaise (not feeling well), fatigue Rapid onset of symptoms Glycosuria blurred vision

Four metabolic problems during DKA

Hyperosmolarity -from hyperglycemia and dehydration Metabolic acidosis -accumulation of ketoacids Extracellular volume depletion -from osmotic diuresis Electrolyte imbalances from osmotic diuresis (loss of Na and K)

Complications: T1D

Hypoglycemia Common for type 1 because they do not make insulin and there's too much insulin and not enough carb load also called insulin shock, insulin reaction, or "the lows" Usually results from mismatch between insulin (error in insulin does) and physical activity and carbohydrate availability Other drugs or alcohol can cause this as well Chloromycetin, Coumadin, MAOS's Benemid, salicylates, sulfonamides-causes

Pharmacologic: T2D

Hypoglycemia agents -lower blood sugar by stimulating or increasing insulin secretion, preventing breakdown of glycogen to glucose by the liver; prevents glycogen being converted to glucose by making cells less resistant to insulin -used to treat individuals with type 2 Clients with type 2 cannot be managed with oral medications when hospitalized due to risk of hypoglycemia from not eating and slow response of these medications to correct hyperglycemia ICU patients -less morbidity with intensive insulin therapy -Decreases risk of postoperative infections -Insulin IV infusions -Maintain normal blood glucose -Frequent monitoring

Postoperative: Diabetes

If NPO, IV dextrose should be administered, with subQ regular insulin q 6hrs T2D- continue to require insulin or may resume oral medication T1D- require reduced insulin as healing progresses and stress diminishes Essential- regular blood glucose monitoring and assessments for hypoglycemia

Hypoglycemia treatment

If the client is conscious and alert: 10-15 g of oral carbohydrate may be given -carbs and protein -15g wait 15 min after 15 min check glucose and continue -Dextrose (rapid active sugar)- juice (half cup) If client has altered levels of consciousness, administer parenteral glucose or glucogon Glucose 1V 50 ml of 50% (D50) given 10 ml over 1 min IVP Glucogon 1 mg SQ, IM or IV (has a short period of action so should be followed up with oral carbohydrates if client is conscious or IV carbohydrate to prevent rebouding

Interventions: T2D

Individualized education about: -Normal metabolism -Diabetes -How diet helps keep blood glucose WNL -How exercise helps lower blood glucose -Self-monitoring of blood glucose -Medications -Manifestations of acute complications

Priority problem: T2D in children

Ineffective Coping (family) or (individual) Chronic pain Imbalanced Nutrition Risk for Injury Risk for Infection Risk for Unstable Blood Glucose

Priority problems: T1D in children

Ineffective Coping (family) or (individual) Chronic pain Imbalanced Nutrition Risk for Injury Risk for Infection Risk for Unstable Blood Glucose

Why does hypoglycemia happen in T1D?

It results from a compensatory autonomic system response and from impaired cerebral function caused by decrease in the glucose available in the brain Severe can cause death

Priority problems (T1D)

Knowledge Deficit Risk for Impaired Skin Integrity Risk for Infection Risk for Injury Risk for Deficient Fluid Volume Sexual Dysfunction Ineffective Coping

Non-pharmacologic: T1D

Management -Balance nutrients, expenditure of energy, dose and timing of meds ADA guidelines -Maintain near normal blood glucose levels -Achieve optimal serum lipid levels (comorbidity with overweight) -Provide adequate calories -Prevent and treat complications of insulin-treated DM -GOAL: Improve overall health with optimal nutrition

When an individual has Type 2 diabetes they should be evaluated for

Metabolic Syndrome: Must have 3 or more symptoms -waist circumference male= above 40 inches Female= above 35 inches Triglycerides above 150 mg/dL HDL Male= below 40 mg/dL Female= below 50 mg/dL Blood Pressure above 130/85 Fasting blood sugar above 100 mg/dL

Nutrition: T1D

Protein intake -15%-20% total daily kilocalorie intake -Low in fat, cholesterol -Lower than most individuals consume -Prevent, delay renal complications Dietary fats -Less than 7% total kcal/day -Cholesterol < 200 mg/day Saturated fat (animal meats) Polyunsaturated (oils of corn, soybean, cottonseed, sunflower) Monounsaturated (peanut oil, olive oil, canola oil) Dietary fiber -Helpful in treating, preventing constipation -Recommended 20-35 g/day Sodium: 1,000 mg per 1,000 kcal -Not to exceed 3,000 mg Diabetic diet plan -Restrict refined sugars -Nonnutritive sweeteners with caution -Alcohol consumption (Signs of intoxication, hypoglycemia similar) (Light beer recommended alcoholic drink) Individualize meal planning

Manifestations HHS

Severe dehydration dry skin and mucous membranes extreme thirst altered LOC (progressing from lethargy to coma) Neurologic deficits may include hyperthermia, motor and sensory impairment, positive Babinski sign, and seizures

Clinical manifestations: T2D

Slow onset Symptoms are similar to that of Type 1 No polyphagia because they still have insulin and still pushing sugar into the cells Do not present with DKA they have insulin, present HHS Fatigue, extreme thirst, frequent urination, extreme hunger, weight loss, infection, slow wound healing, and blurry vision

Surgeries: Diabetes

Surgery alters self-management -Hyperglycemia occurs due to increase in hormones (cortical, glucagon growth hormone) and protein stores are decreased -high risk for infection, delayed wound healing -high risk for fluid, electrolyte imbalances -hypoglycemia, DKA Must be in the best metabolic state before going into surgery to prevent DKA Involves replacing or transplanting the pancreas, pancreatic cells, or beta cells Target blood glucose during surgery is between 110-140 mg/dL- this prevents hypoglycemia (difficult to detect under anesthesia and prevents glycosuria, dehydration, and impaired wound healing) Should be scheduled early in the morning to prevent length of fasting

Collaboration: T1D in children

Team of caretakers -PCP, dietician, certified diabetes instructor, school nurse Federal laws protecting children include: -Rehabilitation Act of 1973 -Individuals with Disabilities Education Act of 1990 (reauthorized 2004) -Americans with Disabilities Act of 1990

Insulin administration

Vials at room temperature up to 4 weeks (stored in fridge) Regular insulin requires no mixing (other types require gentle rolling) Rotate sites (should be at least 1 inch away from previous injection site) Do not massage site after injection- can cause lipoatrophy and interference with absorption Pressure may be applied Techniques for minimizing painful injections Lipoatrophy (atrophy of subQ)- from using same injection site repeatedly, alters absorption; destruction of fat cells Do not shake insulin- shaking breaks down the insulin and gives it air bubbles Mixing insulin- always draw up clear to cloudy because we can put a short acting into the longer acting and it wont mess up the duration as much as the other way around Pressure may be applied

Hemoglobin A1C

determines average BG over approximately the previous 2-3 months When glucose is elevated or control of glucose is erratic, glucose attaches to the Hb molecule and remains attached for the life of the Hb (120 days) Give an idea of how well diabetes is being managed normals- (0-6yrs) <8.5%, (6-12yrs) <8%, (13-19) <7.5 %