Diabetes - chapter 64
how do foot injuries occur?
-barefoot -wearing ill fitting shoes -sustaining thermal injuries from heat -chemical burns from OTC treatments
footwear
-best fitted by a podiatrist -1/2 to 5/8 bigger than your largest toe -heels less than 2 inches -tight shoes = damage -socks should be soft and absorb moisture -change shoes by midday and again in the evening?
autonomic neuropathy
-can affect entire GI system -GERD, delayed emptying, gastric retention, early satiety, heartburn, nausea, vomit, anorexia -sluggish movement of small intestine with bacterial overgrowth all can occur -constipation most common GI problem -urinary issues like incomplete emptying and retention
nutrition therapy and hypoglycemia
-carb replacement per physician -15 to 20g of glucose for levels under 70 -repeat in 15 minutes if manifestations don't get better -30g if less than 50 blood glucose -glucagon IM or sub q for people who can't swallow (unconscious)
CRITERIA FOR DIAGNOSIS OF DM
A1C over 6.5 or 2 hour blood glucose greater than 200 using 75h anhydrous glucose dissolved in water or classic manifestations of hyperlgycemia / random glucose over 200
carbohydrate intake
-carbs are a huge aspect of post meal glucose -managing carbs is the main strategy for glucose regulation control -45% kcal from carbs minimum of 130g/day -fruit, veggies, whole grains, legumes, low fat milk products all contain carbs
preventing hyperglycemic / hyperosmolar state
-caused by hyperglycemia -blood glucose levels are severely high rather than ketone levels are absent or low
WHICH STATEMENT MADE BY A CLIENT WHO IS LEARNING ABOUT SELF INJECTION OF INSULIN INDICATES TO THE NURSE THAT CLARIFICATION IS NEEDED ABOUT INJECTION SELECTION AND ROTATION?
i will stick to my stomach because it is closest to my pancreas. -thigh is OK if that is what you can reach as long as you rotate. -rotate in an area is the right thing to do -you should stick to one sight of your body with rotation so absorption does not change -the stomach is the best because of quick absorption, not for said reason above.
urine ketones
in urine associated with hyperglycemia over 300 is a medical emergency
rapid acting insulin
insulin aspart insulin glulisine human lispro injection
long acting insulin
insulin glargine (kept cold) insuline detemir
hypoglycemia
less than 54 mg -over dosage of insulin -poor meal times -omission of a meal -sick -going hard at the gym -end stage renal issues -alcohol consumption (liver glucose issues) -pallor, diaphoresis, tachycardia, palpitations, nervous, irritability, weak, cool and clammy
focal vs diffuse diabetic neuropathy
DIFFUSE; -most common neuropathies in DM -widespread nerve function and loss of sensory perception -onset slow, both sides of body, motor and sensory nerves, progress slowly, permanent, includes autonomic nerve dysfunction -late complications include foot ulcers FOCAL; -single nerve or nerve group and usually caused by an acute ischemic event leading to nerve damage -ischemic neuropathies occur when blood supply is disrupted -manifestations are sudden, affect one side, self limiting -eye muscle most common -manifestation is pain on one side of the face near the eye, muscle become paralyzed, double vision occurs.
HYPOGLYCEMIA VS HYPERGLYCEMIA
HYPOGLYCEMIA; skin: cool and clammy dehydration: absent respirations: normal mental status: anxious, nervous, irritable, confusion manifestations: weak, double vision, blurred vision, hunger, tachycardia, palpitations glucose: less than 70 ketones: negative HYPERGLYCEMIA; skin: warm, moist dehydration: present respirations: rapid, deep, kussmaul mental status: alert to stuporous, obtunded manifestations: acidosis, hypercapnia, abd cramps, n/v, dehydration, neck vein filling low, orthostatic htn, tachycardia, poor skin turgor glucose: over 250 ketones: positive
risk factors for developing diabetes
a1c over 5.7 OGTT 140-199 first degree relative with it high risk ethnicity (black, latino, native, asian) history of gestational diabetes polycystic ovary syndrome htn history of CVD lazy over 45 years old certain meds (diuretics, anti psychotics) smoking
diagnostic tests
a1c should be under 6.5 FBS at 126 OGTT at 200 random at 200 or above
alpha glucosidase inhibitors
acarbose miglitol -slow carb absorption from intestines -watch for GI upset
nutritional therapy
achieve and maintain body weight goals delay or prevent complications maintain pleasure of eating provide practical tools individualized cultural preferences -carb to insulin ratio 15g = 1 unit = regular -carb to insulin ratio 12.5g = 1 unit = humalog -carbs high in protein should not be used to treat hypoglycemia. -carb and protein if you are an hour or more away from your next meal.
Which assessment finding is identified as a risk for type 2 diabetes mellitus (DM) and cardiovascular disease (CVD)?
Waist circumference of 40 inches or more Abdominal obesity, indicated by a waist circumference of 40 inches or more in men and 35 inches or more for women, is a risk factor for type 2 DM and CVD.The risk for CVD is reduced if the body mass index is maintained at less than 25 kg/m2. A fasting blood glucose level of 90 mg/dL, a systolic BP of 120 mm Hg, and a diastolic BP of 80 mg Hg are normal findings. A fasting blood glucose level of 100 mg/dL or more, or drug treatment for hyperglycemia or hypertension, increases the risk for type 2 DM and CVD.
targets for someone with diabetes
a1c below 7.0 fasting 80-130 peak postprandial at 180
sodium glucose cotransporter 2 inhibitors
canagliflozin dapagliflozin -block reabsorption of glucose from the kidneys
-diagnostic criteria for DM
casual blood glucose over 200 fasting blood sugar over 126 2 hour glucose greater than 200 a1c above 6.5 -must be done on 2 separate occasions
incretin mimetic
exanatide liraglutide
lab diagnostics
fasting lipid profile liver function tests spot urinary albumin to creatinine ratio serum creatinine and estimated GFR thryoid stiulating hormone in patients with t1
rapid acting insulin
lispro aspart glulisine -before meals to control rise from the food onset: 10-30 minutes
DIABETIC KETOACIDOSIS CHART
onset: sudden precipitating factors: infection, stress, insulin erros manifestations: kussmaul, abd pain, dehydration, weight loss, 3 P's, dry skin, sunken eyes, letheragy serum glucose: over 300 BUN: high due to dehydration
short acting insulin
regular insulin -administer 30 to 60 min before meals -u500 used for insulin resistance -u100 for most clients and can be given IV
meglitinides
repaglinide nateglinide -stimulates insulin release from pancreas -post meal admin -monitor for hypo
continuous blood glucose
several days to a week real time measurments every 1-5 minute intervals alarms download to track and the trend expensive not as accurate as blood glucose inserted under the skin
DDP4 inhibitors
sitagliptin saxagliptin linagliptin alogliptin -naturally occuring intestinal incretin hormones promoting release of insulin and decrease secretion of glucagon -respiratory manifestations and pancreatitis
lipodystrophy
skin becomes hardened and has an orange peel appearance -alters insulin absorption -rotate injection sites
While teaching a client about insulin injection technique, the nurse explains that injecting into which area will cause the insulin to be most rapidly absorbed?
stomach Insulin absorption is fastest when it is injected in the abdomen, followed by the deltoid, thigh, and buttocks.
diabetic ketoacidosis
type1; taking too little insulin skipping doses of insulin infection, stress, counter hormones QUIZ 2 MATERIAL.
prediabetes
weight loss target of 7% -increase physical activity -150min a week / 3 days a week -begin metaformin therapy for high risk
self monitoring blood glucose (SMBG)
when prescribed as part of a broad education program you can help there self management for patients taking less frequent insulin injections
vaccine
yearly influenza pneumonia vaccine PPSV23 at age 65: get this shot 1 a year
diabetes self management
knowledge and skills self care decrease complications quality of life
The nurse is providing discharge teaching to a client with diabetes about injury prevention for peripheral neuropathy. Which statement by the client indicates a need for further teaching?
"I can break in my shoes by wearing them all day." Shoes should be properly fitted and worn for a few hours a day to break them in, with frequent inspection for irritation or blistering. People with diabetes have decreased peripheral circulation, so even small injuries to the feet must be managed early. Going barefoot is contraindicated. Tobacco use further decreases peripheral circulation in a client with diabetes.
The nurse is teaching a client with diabetes about proper foot care. Which statement by the client indicates that teaching was effective?
"I must inspect my shoes for foreign objects before putting them on." To avoid injury or trauma to the feet, shoes should be inspected for foreign objects before they are put on. Diabetic clients should not go barefoot because foot injuries can occur. To avoid injury or trauma, a callus should be removed by a podiatrist, not by the client. The diabetic client must wear firm support shoes to prevent injury.
A client recently diagnosed with type 2 diabetes mellitus states, "I don't understand how I got diabetes. I don't eat sugary foods." How does the nurse respond?
"Type 2 diabetes is caused by resistance to insulin or an inability to make sufficient insulin." Type 2 diabetes mellitus (DM) is a progressive disorder in which the person has a combination of insulin resistance and decreased secretion of insulin by pancreatic beta cells. Insulin resistance develops from obesity and physical inactivity in a genetically susceptible person. Heredity does play a major role in the development of type 2 DM, but the nurse cannot assume that is why this client developed type 2 DM; the specific causes of type 2 DM are not known, although there are many genetic and nongenetic causes. Most clients with type 2 DM are obese, with an increased rate of obesity occurring in younger people.
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whole pancreas transplantation
-1 year survival rate over 95% -preformed in 3 different ways; pancreas transplant alone pancreas after kidney simultaneous pancreas and kidney -SPK is ideal procedure for people with DM and uremia
protein intake
-15 to 20% of total daily kcal is appropriate with dm and good kidney function -diet high in protein can improve insulin response -reduced protein in kidney issues -fiber helps with absorption of carbs and should be 25g for females and 38g for males PROTEIN IS NOT A GOOD SOURCE OF CARBS. NOT USED WITH HYPOGLYCEMIA. THE ONLY TIME PROTEIN IS USED AS A SNACK IS WHEN THE NEXT MEAL IS FAR AWAY.
dietary fat and cholesterol
-20-35% of kcal intake -monounsaturated and polyunsaturated fats over saturated / trans fats -limit cholesterol to under 200mg daily -fatty fish per week for n 3 poly fatty acids -trans fat increase risk for cvd found in hard margarine and foods with oil -should be tested 1x annually for serum cholesterol, triglycerides, cholesterol, and LDL
cognitive dysfunction
-65 and over with DM are higher risk of developing all types of dementia as compared with people without it -chronic hyperglycemia and microvascular disease contributes to neuron damage, brain atrophy, cognitive impairment
macrovascular complication; cardiovascular disease
-CVD and DM greatly reduces life span -left ventricular dysfunction and heart failure is common,thrombotic event, MI - r/f for CVD include obesity, high lipid levels, htn, lazy, smoking, family history +, kidney disease shown with albuminuria (presence of albumin in urine), increases risk for CVD and death -complications can be reduced with management of hyperglycemia, htn, hyperlipidemia -140/80 BP or lower for these patients -100mg/dl low density cholesterol OR below 70 with manifestations of CVD -lifestyle modifications include reduce fats, trans fat, cholesterol, increase omega 3 fatty acids, fiber, plant sterols, weight loss, move more -priority nursing care is set on interventions to reduce modifiable risk factors like smoking, diet, exercise, bp control, aspirin use, lipid drug therapy -DM causes subtle manifestations of MI -dypsnea, fatigue, onset nausea and vomit
DM management
-DM is a metabolic disorder resulting from either an inadequate production of insulin (1) or an inability of the body's cells to product enough insulin (2) -type 1 is an autoimmune dysfunction involving destruction of beta cells. -type 2 is progressive condition due to inability of cells to respond to insulin (resistance) and decreased production of insulin by beta cells. -linked to obesity, lazy, heredity -dm can lead to cardio issues, htn, kidney disease, neuropathy, retinopathy, PVD, stroke
thiazolidinediones (TZDs)
-WATCH YOUR HEART, DO NOT USE WITH HEART ISSUES, WARNED BLACK BOX pioglitazone oral - heart, fractures, liver, BC rosigilizatone oral - heart, fractures, liver
risk factors: metabolic syndrome
-abdominal obesity over 40 for men 35 for women -insulin resistance -sedentary lifestyle -htn -elevated lipid and triglyceride levels
cardiovascular autonomic neuropathy (CAN)
-affects sympathetic and parasympathetic nerves to the heart and blood vessels -left ventricular dysfunction, painless MI, exercise intolerance all common -CAN leads to orthostatic hypotension and syncope result of failure of the heart and arteries to adjust during position changes
interventions and DKA
-airway, LOC, hydration status, electrolytes, and blood glucose level -check v/s every 15 minutes until stable -monitor 4 hours once stable
classification of diabetes
-all types of DM= chronic hyperglycemia TYPE 1; -beta cell destruction leading to absolute insulin deficiency -autoimmune -idiopathic (usually born with it, young) TYPE 2; -ranges from insulin resistance with relative insulin deficiency to secretory issues with insulin resistance -insulin resistance or lack or production. greatly related to obesity. gestational DM; -glucose intolerance with onset or first recognition during pregnancy
history gathering and assessment
-ask about risk factors and manifestations r/t diabetes -age is important for type 2 (black or mexican more common) -how large was your baby at birth (GDM) -weight and weight changes (obese, other side of coin DM causes weight loss from lack of energy use)
diagnosis of diabetes
-assessed with blood glucose levels -repeated test to rule out an error -a1c is a standardized test that measured glucose permanently attached to hgb molecule -glucose binds to proteins including hemoglobin, the higher the blood glucose over time the more glycosylated hemolglobin becomes -greater than 6.5 = diagnosis of DM -fasting plasma / blood glucose (FPG/FBG) is used to diagnosis dm in nonpregnant people -no kcal intake for 8 hours prior to (water is OK) -blood sample is obtained before insulin or oral agents have been taken (obviously) -diagnosis is made with 2 separate results greater than 126 -random or casual test greater than 200 is used also with people with severe classic signs oral glucose tolerance testing (OGTT) -most sensitive test for DM diagnosis -used often with GDM -not routinely done for general diagnosis MARKERS OF DM1; islet cell autoantibodies (ICAs) autoantibodies to insulin autoantibodies to glutamic acid decarboxylase -ICAs present in 85-90% of cases of DM1 -C-peptide can indicate beta secretory function -low to absent = 1 as well as late stage 2 DM when ability of pancreas is that bad
random information on nutrition
-avoid sugar sweetened beverages -nonutritive sweeteners to enhance a taste is OK (diet coke) -corn syrup should be avoided with dm because it can increase triglycerides (coke) -moderate alcohol with well controlled is OK -2 drinks for men and 1 for women -exercise can cause hypoglycemia if insulin is not decreased before activity -high levels of insulin can actually cause weight gain in dm1 patients
chronic complications of diabetes
-changes in large blood vessels (macrovascular) -changes in small blood vessels (microvascular) -complications of this result to poor tissue perfusion and cell death -macrovascular issues include; CHD, CVD, PVD -microvascular issues include; nephropathy (kidney), neuropathy (nerves) retinopathy (eye issues) -chronic high blood glucose is the main cause of micro issues and allow premature development of macro issues -smoking, lazy, obesity, htn, high fat and cholesterol all are risk factors -hyperglycemia in poor glucose regulation is critical factor for type 1 DM. -intensive therapy of observation and corrections in sugar levels delays onset of any issue -every percentage point of the A1C, a risk reduction of 25-30% for kidney and eye issues has been shown (A1C is a very sensitive test)
preventing injury from peripheral neuropathy
-clean and inspect feet daily -wear good shoes -don't walk on bare feet -trims toenails properly -reports any nonhealing breaks on tissue -foot injury is the most common complication of diabtes leading to hospitalization -once a foot injury occurs there is a great risk for wound progression leading to amputation -neuropathy = development of foot ulcer -inadequate vascular supply = poor healing
diabetes
-confirm the diagnosis and classify diabetes -detect complications and comorbid conditions -review previous treatment and r/f control in patients with established diabetes -begin patient engagement into their own well being -develop a plan of care
health promotion and maintenance
-controlling DM is a major health goal because of the serious and chronic complications it can cause -nothing can be done to stop type 1 -adopt a low calorie diet -reduce htn with activity -tight control of blood glucose can prevent many complications -go to your Dr. get your tests don't be stupid and skip these things -vision tests -microalbumin levels assessed yearly -healthy weight
motor neuropathy
-damaged nerves of the foot muscles resulting in deformities -these deformities create pressure points causing skin break down and lack of integrity of the skin -claw toe deformity = toes are hyperextended -charcot foot = hallux vagus (turning inward of the great toe) -foot is swollen, warm, and painful
blood glucose therapy goals
-depends on the person -ADA recommends type 1 to be less than 6.5% -premeal glucose levels of 70-130 -postmeal below 180 SLIDES SAY OTHERWISE. SLIDE SAYS LESS THAN 7% AND 80-130
glucose regulation and homeostasis cont.
-during fasting (sleeping 8hrs) maintain glucose range of 60-150 by a balance of uptake and production of glucose by the liver. - food = glucose which needs to be regulated or else damage is caused to the body. insulin in secreted by the pancreas = key to cells of the body that allows the entrance of the glucose to be used and thus removed from the blood. -insulin keeps blood glucose levels in a balanced range and also has an effect on glycogen, protein and lipids, and muscle activity -incretin hormone is secreted in response to food in the stomach, increases insulin production, inhibit glucagon secretion, slow rate of gastric emptying (preventing hyperglycemia post meal)
the endocrine pancreas
-endocrine functions are r/t blood glucose -1 million small glands, islets of langerhans -alpha = secrete glucagon -beta = insulin and amylin -glucagon is a hormone that acts opposite of insulin. it prevents hypoglycemia by its triggered release from cell storage sites. -insulin from the body prevents hyperglycemia by allowing body cells to take up, use and store carbs (key to the cell allowing flow of energy) -insulin is secreted daily into the liver. -low levels during fasting (basal insulin) -increased after eating (prandial) which is a burst of insulin within 10 minutes of eating.
DPP-4 inhibitors
-enzyme breaking down natural gut hormones and decreasing liver glucose production sitagliptin oral - acute pan saxagliptin oral - acute pan linagliptin oral - acute pan alogliptin oral - acute pan
while assessing a client who had diabetes for 15 years, the nurse finds that he has decreased sensory perception in 2 feet. what's your first action?
-examine the feet for any damage that might have occurred
prevention strategies
-excess insulin -deficient intake of food -exercise (usually in type1) alcohol intake (inhibits liver glucose) -these are the 4 most common causes -always have carbs near by -
client education
-exercise and good nutrition are imperative for preventing or controlling diabetes carbs: 45% of daily intake protein: 15-20% daily depending on kidneys unsaturated fats/polysaturated: 20-35%
preventing hypoglycemia
-fall below 70 a sequence of events start with counteregulatory hormones -manifestations include sweating , irritability, tremors, anxiety, tachycardia, and hunger serve as an early sign of hypoglycemia -confusion, paralysis, seizure and coma occur from brain glucose deprivation -insulin decreases at about 83mg in a healthy person -counter regulatory hormones kick in at about 67mg
absence of insulin cont.
-fat breaks down when there is a deficiency in insulin, releasing fatty free acids -conversion of fatty acids to ketone bodies provides a backup source of energy -ketones are NOT NORMAL / HEALTHY and can collect in the blood leading to ketoacidosis
management of hypoglycemia at home
-for mild hypo (hungry, irritable, shaky, weak, headache,fully conscious) -10 to 15 carbs you may use; glucose tablet or glucose gel 1/2 cup of fruit juice 1/2 cup of non diet soft drink 8 oz skim milk 6-10 hard candies 4 cubes of sugar 4 tb of sugar 6 saltines 3 graham crackers 1 tb on honey or syrup -re test BS in 15 minutes -repeat if symptoms don't go away -eat a small snack or carbs and protein if next meal is more than an hour away
drug therapy and pain management
-gabapentin -pregabalin -SNRI duloxetine
hormones that INCREASE (counterregulatory hormones increasing blood sugar)
-glucagon is the main hormone -epineephrine -norepinephrine -growth hormone -cortisol -combined efforts of this and insulin result in glucose regulation and keep ranges in 60-100 to support brain function -blood glucose falls = insulin stops and glucagon starts. glucagon causes glucose release from the liver. liver glucose is made with breakdown of glycogen into glucose and converted into amino acids into glucose. -when liver glucose is not there, breakdown of fat (lipolysis) and breakdown of proteins (proteolysis) provides the fuel - liver glucose / fat / proteins all sources of fuel
glucose regulation and homeostasis
-glucose is main fuel for the CNS cells -brain needs a continuous supply of this -glucose is stored inside cells as glycogen in the liver and muscles -free fatty acids stored as triglycerides in fat cells -fat is more efficient of energy as 9kcal per gram (not good energy, keto) -protein and carbs have 4kcal per gram -during prolonged fast or illness, proteins are broken down for amino acids converted into glucose
ongoing assessment
-glycosylated hemoglobin assays are useful because you can not lie to this test -shows average blood glucose during 120 days or the life of the RBC -should be done twice a year -glucose and amino groups = fructosamine -same as A1C but shorted time frame -GSA GSP and fructosamine
male erectile dysfunction
-higher rate upon having this problem and occurs 10-15 years earlier in men with DM -r/t to poor blood glucose regulation, obesity, htn, smoking, presence of other vascular issues
hyperglycemia manifestations and management
-hot, dry skin, fruity breath -encourage oral intake of sugar free things to prevent dehydration -administer insulin as ordered -restrict exercise when glucose over 250 -test urine for ketones
blood glucose control in hospitalized patients
-hyperglcemia in patients in the hospital can occur for many reasons -"stress hyperglycemia" -can also occur from a decline in basic level glucose regulation caused by illness, decreased movement, withholding antidiabetic meds, or other reasons -hypoglycemia defined as below 40mg is an independent r/f for mortality
dawn phenomenon
-hyperglycemia in the a.m -overproduction of the growth hormone or cortisol -blood sugar at 2-3 am
somogyi effect
-hyperglycemia when you wake up -counter regulatory responded when your blood glucose dropped low during your sleep -reduce bed time insulin -headaches, sweats, or nightmares -monitor 2-4 am again at 7 am HERE SAYS REDUCE INSULIN BOOK SAYS NIGHT TIME FOOD.
complications of insulin therapy
-hypoglycemia is a complication -lipoatrophy (loss of fat tissue in areas of repeated injection) -lipohypertrophy (increased swelling of fat that occurs at the site of repeated injections)
insulin resistance
-impaired fasting glucose levels 100 to 125 -impaired glucose tolerance 140-199 -a1c level 5.5 to 6.0
rejection management
-in most cases of rejection, kidney issues arrive before pancreatic issues -increase in creatinine indicates rejection of both transplant kidney and the pancreas -urine amylase level of 25% decrease sign of rejection
more manifestations of lack of insulin
-increased rate and depth of breath to "blow off" co2 and acid from the body -kussmaul respirations is a sign of severe insulin deficiency. "rotting fruit" breathe -lack of insulin also causes K deficiency -excessive K is excreted in the urine, leading to low serum levels. -this isn't very accurate because it can also be high due to a shift from cells to blood
drug therapy
-indicated when exercise, diet and stress management has not been well -drugs are not an alternative to diet and exercises@!
absence of insulin
-insulin for glucose regulation is needed to move glucose into body tissues -lack of insulin in diabetes from lack of production or insulin at its cell receptor prevents cells from using glucose for energy -body will then break down fat and protein in an attempt to get energy and increase levels of counteregulatory hormones -glucose build up in the blood causes fluid and electro issues, with classic signs of hyperglycemia; polyuria (piss out this sugar) polydipsia (pissing out fluids, I'm thirsty) polyphagia (cells are hungry) -despite eating a normal diet, these people are hungry because cells are signaling they are low on energy because the key is missing (insulin)
long acting insulin
-insulin glargine - insulin detemir -once daily anytime during the day but always at the same time
preventing high risk conditions
-keep your blood glucose levels normal as possible -poor blood glucose control increase risk for neuropathy and future amputation -infection impairs glucose regulation, leading to higher levels and reduced immune defenses -stop smoking
urine tests
-ketone bodies are a product of fat metabolism, presence of moderate to high ketones indicate a lack of insulin and body is looking elsewhere -hyperketonuria is a medical emergency -urine tests for ketones should be performed during acute illness or stress, blood glucose over 300, during pregnancy, manifestations of ketoacidosis are present
acidosis management
-key feature of DKA is a elevation in anion gap -blood ketone concentration is measured in serum b hydroxybutyrate -normal anion gap is 7-9 but with DKA it can become 10-20 indicating metabolic acidosis
midterm prep
-lack of insulin causes K deficiency. if someone comes in with severely elevated blood glucose they will most likely be dehydrated as well as have a low K level. give these people fluids, correct there K imbalance, than give them insulin. rationale is you need to make sure they can have proper kidney function and output before you give them K or insulin. also need to correct K dysfunction prior to insulin to correct any electro imbalances. -protein is NOT carbs. avoid chicken and eggs. they are a bad alternative. -if someone needs carbs, bread, fruit are good examples -someone with ketones should NOT work out. people with t1 are more tricky to go to the gym. t2 gym is helpful because it can make insulin less resistant if you lose some weight. just give yourself less insulin prior to working out with t2. blood glucose over 250 and you should avoid working out. ketones present don't work out.
dehydration and diabetes
-leads to; hemoconcentration (low dilution, severe thirst) hypovolemia (blood volume low) concentrated blood poor tissue perfusion hypoxia especially to the brain
ulcer formation
-plantar ulcers (on the sole) occur from standing or sitting and calluses can form -ulcers usually occur around the great toe, under the metatarsal heads, top of claw toes -once these ulcers formation they are a pain in the ass to treat because there is so much nerve and vessel damage
microvascular complication; vision issues
-legal blindness (20/200 or less) is 25 times more likely with DM -relation to duration, 20 years or more high likely you have eye problems -retinal blood vessels begin to leak leading to retinal hypoxia -venous beading is abnormal appearance of retinal veins with swelling and constriction resemble links of a sausage -proliferation diabetic retinopathy is the growth of new retinal blood vessels aka neovascularization -retinal cells secrete growth factors stimulating formation of new blood vessels in the eye (amazing compensation) -these new vessels are thin, fragile, and bleed easily, leading to eye hemorrhages and vision loss -sensory perception loss also occurs -central vision can be impaired by edema, hard exudates at the center of the retina -this problem is the main cause of vision loss -RANIBIZUMAB (LUCENTIS) can improve vision with edema -routine eye exams, every year -hyperglycemia = blurred vision -hypoglycemia = double vision
autonomic neuropathy
-loss of normal sweating and skin temp regulation -dry, thinning skin results
meglitinide analogs
-lower fasting plasma glucose by triggering release from beta cells -repaglinide -nateglinide
sulfonylurea agents
-lower fasting plasma glucose levels by triggering release of insulin from beta cells -interacts with many drugs, be careful -glipizide (glucotrol) oral -glimepiride (amaryl) oral
nutrition therapy
-meal plan, education, counseling programs -registered dietitian should be a member -culture, finances, lifestyle all involved -no 1 plan is for everyone, depends on there blood glucose, total lipids, a1c levels -taking insulin and you need to coordinate your timing of food
screening for DM
-measurement of islet cell antibodies may i.d people who are risk for DM1 -testing for prediabetes should be done in older than 45 and obese greater than 25 BMI -younger than 45? overweight with additional r/f for diabetes (lazy, mom has it, eat like shit) -A1C and fasting plasma glucose levels is is usually done for screening
CULTURED CONSIDERATIONS CHART
-minorities with a greater burden -african american rates are higher -kids are lazy, tv, home on phones
foot care
-monitor feet daily with proper care including nail and skin care -check between your toes -wash feet daily with warm water and soap. dry well -apply mositure cream to feet after a bath; none between your toes -change into clean cotton socks daily -do not wear same pair of shoes 2 days in a row. wear only shoes made of breathable material like leather or cloth -check your shoes before putting them on -purchase shoes with plenty of room for your toes -wear socks to keep your feet warm -trim nails straight across with a nail clipper. smoother the nails with an emery board -call HCP if any issues arrives -do not treat blisters, sores, infections at home -do not smoke -do not step into bath tub without checking temp -do not wear sandals with open toes or straps between toes -do not soak your feet
somogyi phenomenon
-morning hyperglycemia from the counteregulatory response to nighttime hypoglycemia resulting in release of liver glucose. -managed by ensuring adequate dietary intake at bedtime
incretin mimetics
-natural gut hormones, glucagon like substance albiglutide sub q - pancreatitis, thyroid cancer 1x weekly exenatide sub q - pan, SJS liraglutide sub q - pan, thyroid cancer
operative procedure
-new pancreas is put in the pelvis and the old one is left in place
dawn phenomenon
-nighttime release of growth hormone that causes release of liver glucose resulting in blood glucose elevations at about 6 am -managed by providing more insulin for the overnight period
kidney disease and diabetes
-normalize BP -correcting hyper lipids -dietary protein restricted -control of htn is critical -kidney function tests with serum creatinine and GFR measurments yearly -microalbuminuria is performed for type 1 over 5 years or type 2 starting at diagnosis -persistent albuminuria in the range of 30-300mg/hour is the earliest stage of nephropathy in type 1 and a marker of development for type 2 -albumin levels over 300 great risk for end stage kidney disease
nonsurgical management and diabetes
-nutrition interventions -blood glucose monitoring -exercise program -drugs to lower glucose levels -A1C below 6.5 -premeal glucose 70-130 -peak after meal less than 180 -these are goals of the diabetes associated
sensory neuropathy
-pain, tingling, or burning sensation -numbness and reduced sensory perception -without normal sensation you do not notice an injury to the foot and in turn make the injury worst.
surgical management and diabetes
-pancreas transplant -eliminates need for insulin or glucose monitoring -lifelong drug therapy to prevent graft rejection -anti rejection meds can actually cause hyperglycemia so this can not be done with someone who has serious progressive issues
microvascular complications; diabetic nephropathy
-pathologic changes to the kidneys reducing their function leading to failure -leading cause of CKD and ESKD -R/F include 10 to 15 year history with DM, poor glucose control, uncontrolled htn, genetic predisposition (serum uric levels higher, tumor necrosis factor receptors are higher) -should be prevented and the progression to ESKD should be very delayed -keep a healthy blood sugar, use drug therapy to protect the kidneys -ACE and ARBS protect the kidneys well -kidney disease causes progressive albumin excretion and declining GFR. -early manifestations of nephropathy include microalbuminuria (small amounts of albumin in urine) and elevated serum uric acid levels -annual testing for microalbuminuria is rec. for type 1 and for at least 5 years and anyone with type 2 -chronic high BS, cause htn in kidney blood vessels and excess kidney tissue perfusion -increased pressure damages the kidneys -vessels narrow and become leaky -decreased kidney o2 perfusion -process worsens over time scarring glomerular blood vessels and loss of urine filtration
kidney function tests for microvascular issues
-persistent albuminuria in range of 30 to 299 in 24 hours in indicator of early stage nephropathy -serum creatinine is used to estimate kidney function and GFR rate and to help stage the disease if any -urine glucose is not accurate and is not done for monitoring DM management
incidence and prevalence
-prediabetes; defined as impaired fasting glucose or impaired glucose tolerance or an A1C between 5.5-6.0% -fasting BS of 100-125 is not a good thing -people with prediabetes are at severe risk for developing dm2 -almost 1/3 of US population has some sort of diabetes pre,1,2 -more common in men compared to women
alpha glucosidase inhibitors
-prevent after meal hyperglycemia by inhibiting enzymes in the intestinal tract, reducing rate of digestion of starches acarbose oral - abdominal issues, kidney miglitol oral - abd. issues, kidney
blood glucose monitoring
-prior to meals, snacks, at bed time -occasionally post prandially -prior to exercise -when they suspect a low reading -after treating hypoglycemia -prior to critical tasks like driving
microvascular complication; peripheral neuropathy
-progressive deterioration of nerve function that results in loss of sensory perception -common complication of DM and often involves all parts of the body -pain or loss of sensation occurs -factors of DPN; -hyperglycemia, long duration of DM -damaged blood vessels leading to reduced neuronal o2 -autoimmune neuronal inflammation -increased genetic susceptibility -smoking and alcohol abuse
diabetic screening
-r/f include: obesity, htn, lazy, high lipids, smoking, genetic history, ethnic group, women with POS, or delivered fat babies -screening is rec. for anyone over 25 as a BMI and older than 45, or if a child is overweight with additional risk factors -screening is done with fasting serum glucose levels or a1c
benefits of exercise
-results in better blood glucose regulation and reduced insulin reqs. -exercise increases insulin sensitivity causing better cell uptake of glucose promoting weight loss
Diabetes general info
-results in poor glucose regulation and is a major health concern -htn and hyperlipidemia are complications by this -DM is leading cause of blind, end stage kidney disease, foot/leg amputations -complications can be controlled with glycemic control and management of htn and hyperlipidemia -nursing priorities = achieve and maintain lifestyle changes to prevent lifelong issues -DM is a chronic metabolic disease and thus requires behavioral changes for management
WHICH HEALTH PROBLEMS ARE CONSIDERED RESULTS OF MICROVASCULAR COMPLICATIONS FROM LONG TERM OR POORLY CONTROLLED DIABETES?
-retinal hemorrhage and male ED -wasn't obesity, hyperglycemia, heart failure, ketoacidosis, HHS
adjustments for diabetes complications
-retinopathy or nonproliferative retinopathy can cause some strains on your exercise and vigorous aerobic or resistance exercises should be avoided -retinopathy = no valsalva maneuver -proper footwear so you don't put damage on your feet -when ketones are present, you should not exercise. ketones indicate an insulin issue
NANDA priority and DM
-risk for injury r/t hyperglycemia -potential for impaired wound healing r/t endocrine and vascular changes -risk for injury r/t diabetic neuropathy
macrovascular complication; cerebrovascular disease
-risk for stroke is 2-4x higher with DM -htn, hyperlipids, nephropathy, PVD, alcohol and smoking all also increase risk for stroke -DM affects stroke outcomes. more likely to suffer irreversible brain damage with carotid emboli than without DM
HOW IS HYPOHGLYCEMIA CONTROLLED IN A HEALTHY PERSON AS THEY SLEEP FOR 8 HOURS?
-secretion of glucagon prevents hypoglycemia by promoting glucose release from liver storage sites. -was not lipolysis, proteins, or metabolism being slow.
peripheral neuropathy management
-should be evaluated yearly -full foot assessment with a sensory exam with semmes weinstein monofilaments shows the risk for ulcers -it uses 10-g force and you should be able to easily feel this -apply monofilament to designed area of the foot -apply pressure until they feel it or the filament bends -quickly remove it and do not touch another area -do not do this to areas with damage
amylin analogs
-similar to amylin the natural hormone produced by beta cells. lowers blood glucose levels by delayed gastric emptying pramlintide sub q- hypoglycemia, n/v
metabolic syndrome
-simultaneous presence of metabolic factors known to increase risk for dm2 and CVD abdominal obesity; 40 for men 35 for women hyperglycemia; fasting BS over 100 abnormal a1c; 5.5-6.0% htn; 130/85 or on drug treatment for htn hyperlipids; 150 or more for triglycerides or high density cholesterol less than 40 for men and 50 for women -any one of these health problems increase rate of atherosclerosis and stroke, CHD, early death -lifestyle changes need to be made
wound care
-standards is a moist wound environment, debridement of necrotic tissue, and elimination of pressure -eliminate pressure on infected area in huge -do not wear shoes on affected foot -offloading things like total contact casting, half shoes, removable cast walkers, wheelchairs and crutches can help offload the force away from ulcer sites and pressure points
carbohydrate counting (CHO)
-this is the biggest affect on post meal glucose and should be well monitored -formula for this is 1 unit of insulin for each 15g of carbs -read your labels to determine this
most common causes of hypoglycemia
-too much insulin compared to food intake -give a fast acting insulin before you eat and you start to talk to family -wrong type of insulin at wrong time -decreased food intake from a missed dose -delayed gastric emptying -decrease liver glucose production with alcohol digestion -increased insulin sensitivity post getting healthy
CDC
-type 2 accounts for 90-95% of all diabetes causes -leading cause of kidney failure, low limb amputations, adult onset blindness
preventing diabetic ketoacidosis
-uncontrolled hyperglycemia, metabolic acidosis, increased production of ketones -occurs most often in patients with type 1 but also with 2 under trauma, surgery, infection (stress) -most common percipitating factor of DKA is infection -classic manifestation of DKA is polyuria, polydipsia, polyphagia, vomit, abd pain, dehydration, weak, confused, shock, or coma (all signs of hyperglycemia) -as ketones raises, ph lowers -kussmaul respirations occurs
insulin therapy
-used for 1 and maybe 2 -older people may have visual issues, coordination impairment
exercise therapy
-works well for carb metabolism and insulin sensitivity -people with dm1 need to figure out a plan to work out because muscles are burning energy (glucose) and they release glucagon and epinephrine causing hyperglycemia -absence of insulin causes fatty acids to become a source of energy resulting in ketone bodies -muscles also can burn glucose (energy) causing hypoglycemia and the glucose release from the liver is not sufficient
acute complications of diabetes
3 glucose related emergencies; -diabetic ketoacidosis (DKA) lack of insulin and ketosis (buildup in blood) -hyperglycemic hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration -hypoglycemia from too much insulin or too little glucose. -all 3 problems require ER treatment and can be fatal with poor intervention.
The nurse has just taken a change-of-shift report on a group of clients on the medical-surgical unit. Which client does the nurse assess first?
Client taking glyburide (Diabeta) who is dizzy and sweaty The client taking glyburide (Diabeta) who is dizzy and sweaty has symptoms consistent with hypoglycemia and should be assessed first because this client displays the most serious adverse effect of antidiabetic medications. Although the client taking repaglinide who has nausea and back pain requires assessment, the client taking glyburide takes priority. Metformin may cause abdominal cramping and diarrhea, but the client taking it does not require immediate assessment. Ankle swelling is an expected side effect of pioglitazone.
The nurse is caring for a client with continuous glucose monitoring and obtains an elevated reading. What is the first action by the nurse?
Confirm the results with a finger stick test. Continuous glucose monitoring is meant to supplement, not replace, finger stick tests. Insulin should be given only after confirming the results of any of the continuous glucose monitoring systems. CGM provides information about the current blood glucose level, provides short-term feedback about results of treatment, and provides warnings when glucose readings become dangerously high or low.
What method must the client with diabetes use with regard to insulin safety?
Discard any unused insulin after 28 days. The client must discard any unused insulin after 28 days because a slight loss in potency may occur after the bottle has been in use for more than 30 days, even when the expiration date has not passed. The bottle or the prefilled syringe may be rolled gently between the hands, but not shaken vigorously before administration, to prevent loss of potency. Prefilled syringes must be stored upright, with the needle pointing upward, to prevent clogging of the needle. Unused insulin must not be exposed to temperatures below 36° F (2.2° C) to prevent loss of drug potency.
A client has 0700 fingerstick blood glucose readings of 353-286 for 3 mornings in a row, and the nurse is concerned the client may have dawn phenomenon. Which finding is consistent with this phenomenon?
Early morning glucose elevations Dawn phenomenon results from a nighttime release of growth hormone causing blood glucose elevations around 5-6 AM. This is resolved by administering more insulin for the overnight period. All individuals have some degree of postprandial glucose elevation; release of insulin from the pancreas or exogenous insulin resolves this issue. Somogyi phenomenon is early morning hyperglycemia secondary to nighttime hypoglycemia. A client may develop hypoglycemia at bedtime if sufficient calories are not consumed relative to the dinner/evening insulin prescription.
Which outcome is essential for the nurse to include in the plan of care for a client who has been newly diagnosed with diabetes mellitus?
Ensuring the client recognizes the signs and symptoms of hypoglycemia Some symptoms of hypoglycemia include diaphoresis, tremor, anxiety, confusion, hunger, loss of consciousness, and even seizure and brain damage; therefore, it is essential for the client to recognize these symptoms and intervene immediately in order to prevent severe hypoglycemia. Diabetes education is complex and the nurse must first distinguish and emphasize survival skills information from the material the client can learn after discharge. Inspecting the feet daily is important to detect early signs of tissue damage, especially when neuropathy is present; however, it does not take priority over learning to recognize and treat hypoglycemia. The client who needs insulin will return-demonstrate insulin administration; it is not essential the family do so prior to discharge. The client's diet may be based on units of carbohydrate measurement; this does not take priority over managing hypoglycemia, which is potentially life-threatening.
insulin therapy chart
FA = onset 10-20min; peak 1-2 hrs; duration 3-6 hrs (right before eating) SA = onset 1/2-1 hr ; peak 2-4 hrs; duration 5-8 hrs (meal on its way) INT = onset 1-2 hr; peak 4-12 hrs; duration 16-24 hrs (between meals) detemir = onset 1 hr; peak 6-8 hrs; duration 5-24 hrs (1x daily) glargine = onset 2-4 hrs; no peak; duration 24 hrs (1x daily) 10 20 30 1 1 2 1 2 4 (onsets in order) 1 to 2, 2 to 4, 4 to 12, 6 to 8, none (peak)
BLOOD GLUCOSE LEVELS
FASTING (8 HOURS); less than 100mg -level over 100 indicates impaired fasting glucose GLUCOSE TOLERANCE TEST; less than 140mg -over 140 indicates impaired glucose tolerance A1C TEST; 4-6% -5.7-6.4 = increased risk of diabetes -8 or above = poor diabetes control and these people need to be addressed
Which statement about prediabetes is correct?
It describes people at risk for type 2 diabetes who have a fasting glucose level of 100-125 mg/dL. An individual with a fasting glucose level between 100 and 125 mg/dL has prediabetes, which is associated with an increased risk for developing type 2 diabetes. Type 1 diabetes is usually diagnosed in people younger than 30 years of age and is associated with the absence of insulin. Individuals with type 1 diabetes are always insulin-dependent; those with type 2 diabetes may become insulin-dependent as the beta cells lose function and/or insulin resistance worsens. The person with type 1 diabetes is dependent on insulin for glucose transport as the pancreas is unable to produce endogenous insulin. These individuals may also be overweight and have metabolic syndrome, a risk for cardiovascular disease. Insulin resistance and/or decreased secretion of insulin by pancreatic beta cells are characteristic of type 2 diabetes.
The nurse is caring for a client with diabetes. What distinguishing characteristic of glucagon must the nurse be aware of?
It triggers the release of glucose from cell storage sites. Glucagon is a "counterregulatory hormone" that prevents hypoglycemia by triggering the release of glucose from cell storage sites. It is secreted by the alpha cells of the islets of Langerhans, while insulin is secreted by the beta cells. Insulin prevents hyperglycemia by allowing the body to take up, use, and store carbohydrates. Glucagon is released when glucose levels fall and insulin secretion stops. Insulin is secreted within 10 minutes of ingestion of food and continues to be secreted until the blood glucose level is normal.
Which medication taken by a client with diabetes mellitus will protect the kidneys and help prevent diabetic nephropathy?
Lisinopril (Zestril) Drugs that protect the kidneys are the angiotensin-converting enzyme (ACE) inhibitors and the angiotensin receptor blockers (ARBs); lisinopril is an ACE inhibitor. Propranolol is a beta-adrenergic blocking agent, which can be used for hypertension, but does not possess protective effects for the kidneys. Metoclopramide is used to promote gastric emptying for diabetic clients with gastroparesis. Digoxin is a glycoside to slow and/or strengthen the force of cardiac contraction in clients with atrial fibrillation or heart failure; it does not protect the kidneys from diabetic nephropathy.
intermediate acting insulin
NPH insulin -used for between meals and night -not used before a meal
etiology and genetic risk
TYPE 1; -autoimmune disorder in which beta cells (insulin producer) is destroyed -body fails to recognize this cell as normal TYPE 2; -progressive disorder in which person has combo of insulin resistance and decreased prod. of beta cell secretion -insulin resistance (reduced cell response) develops from obesity and physical inactivity in a genetically susceptible person -resistance occurs before onset of dm2 often accompanied by cardiovascular r/f -many of these patients are obese
TYPE 1 VS TYPE 2 CHART
TYPE 1; age = younger than 30 symptoms = abrupt onset, 3 P's, losing weight etiology = viral infection patho = pancreatic beta cell autoimmune issue antigen patterns = HLA;DR, HLA,DQ antibodies = ICAs present at diagnosis nutritional status = usually non obese insulin = 100% necessity medical nutrition therapy = mandatory TYPE 2; age = adult onset, 50s symptoms = thirst, blurred vision, fatigue, neuro complications etiology = not known patho = insulin resistance dysfunctional pancreatic beta cell antigen = none antibodies = none nutritional status = usually obese insulin = required for 20-30%
expected findings for hyperglycemia
blood glucose over 250 -polyuria : excessive urine production -polydipsia: thirst due to dehydration -polyphagia: hunger due to lack of cells to utilize glucose and body's use of protein and fat for energy (which causes ketosis) -the client can show weight loss -ketones accumulate in blood due to breakdown of fatty acids when insulin isn't used, acidosis -kussmaul respirations -fruity breath -headache, nausea, vomit, abd pain, fatigue, weakness, vision changes, slow healing wounds, decreased LOC and seizures / coma late signs
pain management and neuropathy
diabetic neuropathy can feel like; burning, muscle cramps piercing, stabbing, darting pain metatarsalgia (feels like your walking on marbles) allodynia (pain in response to normally nonpainful stimuli) tingling, numbness, loss of proprioception in lower extremities
second generation sulfonylureas
glipizide glimepiride glyburide -insulin release stimulation from pancreas causing a decrease in blood sugars -monitor for hypoglycemia -30 min before meals
counter regulatory hormones
gluacagon cortisol growth hormone epinephrine norepinephrine
clinical manifestations of hyperglycemia
glucosuria polyuria (pee alot) polydipsia (dehydrated, drinking tons) polyphagia (i'm hungry)
DM defined
group of metabolic diseases characterized by increasing levels of glucose in the blood -normal is 70-100
intermediate acting insulin
isophane insulin NPH injection humulin N novolin N relion N humulin 70/30 novolin 70/30 relion 70/30 humulin 50/50 novolog mix 70/30 humalog 75/25
biguanide
metformin -reduces production of glucose by the liver -lactic acidosis -take with food -monitor GI distress -KIDNEY FUNCTION
biguanides
metformin oral works on the hepatic glucose production -abdominal discomfort -contrast material and can induce AKI
treatment of hypoglycemia
mild = shaking, weak, hungry -given carbs 15g check again in 15 minutes moderate = cool, clammy, rapid pulse, drowsy -15-30 carbs and repeat until relieved severe = less than 20mg; unconscious -1mg glucagon another 10min another 1mg
hypoglycemia manifestations and management
mild shaking, mental confusion, sweating, palpitations, headache, lack of coordination, blurred vision, seizure , coma -avoid insulin overdose, exercise caustiously, alcohol consumption -don't skip meals and check your levels - if you become unconscious administer glucagon and with out results in 10 minutes repeat -call the hcp place in lateral position
thiazolidinediones
pioglitazone -reduces production of glucose in the liver -watch for fluid retention
amylin mimetic
pramlintide -amylin hormone found in beta cells
ketone checks
presence of ketones in the urine occurs with the breakdown of dats and is an indication of DKA which is never a good thing -type 1; sick, blood glucose over 250 (book says 300)
short acting insulin
regular human insulin injection humulin R
