NPH(Humulin N, Novolin N, ReliOn N)
lispro, aspart, flulisine
Regular(Humulin R, Novolin R, ReliOn R)
high BG symptoms (hyperglycemia)
thirst, hunger, frequent urination, fatigue, nausea, blurred vision, HA, nervousness, confusion
low BG symptoms (hypoglycemia)
shakiness, sweaty, hunger, anxiety, nervousness, confusion, acting angry or irritable, slurred speech, HA
Causes of hyperglycemia
too much food, too little exercise, too little medicine, stress, illness, injury, short time between meals and snacks
Causes of hypoglycemia
too little food, too much medicine, more activity than usual, too long between meals or snacks, alcohol
Onset: 15 minutes
Peak: 60-90 minutes
Duration: 3-4 hours
Onset: 30-60 minutes
Peak: 2-3 hours
Duration: 3-6 hours
Peak: 4-10 hours
Duration: 10-16 hours
Onset: 1-2 hours
Peak: no pronounced peak
Duration: 24+ hours
Humulin 70/30, Novolin 70/30, ReliOn 70/30
lispro protamine/lispro 75/25
Humalog mix 75/25
aspart protamine/aspart 70/30
Novolog Mix 70/30
stimulate release of insulin from pancreatic islets; decrease glucogenolysis and gluconeogenesis; enhance cellular sensitivity to insulin. increases insulin secretions
stimulate a rapid and short-lived release of insulin from the pancreas
decreases rate of hepatic glucose production; augments glucose uptake by tissues, esp. muscles (lower risk of hypoglycemia)
delay absorption of glucose from GI tract
glucose uptake in muscle; decreases endogenous glucose production (timing for meals not as important)
Dipeptidyl Peptidase-4 (DDP-4) inhibitors
enhances the incretin system, stimulates release of insulin from pancreatic B bells, and decreases hepatic glucose production
combination of metformin and glyburide
combination of rosiglitazone and metformin
combination of metformin and glipizide
combination of pioglitazone and glimepiride
stimulates release of insulin; decreases glucagon secretion; increases satiety, decreases gastric emptying
decreases gastric emptying; decreases glucagon secretion; decreases endogenous glucose output from liver; increases satiety
which oral med classifications are given before meals?
which oral med classification is faster than sulfonylureas?
which classification do you hold if they don't eat?
which classification helps the "leaky faucet"
which type do you take with first bite of food (starch blocker)?
which type is for insulin resistance, makes insulin work better?
type 1 drug therapy
1 from basal, 1 from bolus
type 2 drug therapy
1 from basal OR 1 from bolus
type 1 (oral drug therapy)
no oral insulin
shot of long acting and oral pill to cover meals
when mixing insulin in syringe remember
clear to cloudy
do not mix
which drug therapy is dose and eat or eat and dose
which drug therapy mimics postprandial rise and fall of insulin
intermediate-acting is usu. given _____ time(s) a day
Location of pancreas
risk factors for DM
obesity, genetics, chronic pancreas disorders, meds (steroids)
Alpha cells produce
glucagon turns into
beta cells produce
delta cells secrete
inhibits glucagon and insulin
glucagon is used for
insulin is the
key to the cell to let glucose inside the cell
metabolic disorder of the pancreas that affects fat, CCHO, and protein metabolism
Prevalence of DM
adults are more prone than children, 7th leading cause of death in the USA, African Americans-high prevalence
when cells don't have glucose they go into starvation mode and attack
muscle, organs, and even bone
quick source of energy
longer lasting energy
waste product of protein metabolism in the body
Function of insulin
key to open the cell to let glucose in
Production of insulin takes place
in the pancreas by the beta cells
Type 1 DM (IDDM or juvenile)
pancreas does not secrete insulin, usually caused by destruction of beta cells, requires insulin injections, onset is rapid, theory is that it is a auto immune disorder, hereditary link, prone to get ketoacidosis
Type 2 DM (NIDDM or adult onset)
some insulin production, largest cause HEREDITY, obesity.
occurs during pregnancy, usually resolves itself AFTER THE BABY IS BORN, more susceptible to having DM later in life, may require insulin during pregnancy
GTT (glucose tolerance test)
requires to drink a sugary drink and then the blood and urine is tested every hour
impaired glucose intolerance
blood sugar is above normal without meeting other DM requirements
BS 140-200 after 2 hours =
IFG (impaired fasting glucose)
after fasting for 8 HOURS a result of 10-126=impaired fasting glucose
Other causes of DM
chronic pancreatitis, prolonged use of steroids, diuretics, thyroid medication
MODY (maturity onset diabetes of the young)
inherited insulin impairment that occurs before age 25
S/S of DM
polydyspia, polyuria, polyphagia, glycosuria, nocturia, fatigue, blurred vision, abdominal pain, headaches
Random Blood sugar
no preplanning; results >200=DM
Fasting Blood Glucose
obtain after 8 hours fasting; results 70-110= normal
obtain 2-4 hours after a meal; results >140=DM
drink high sugary drink and test urine and blood 3 hours after; results glucose levels return normal in 2-3 hours and urine negative for glucose= normal
lab draw test for last 90-120 days; 7%= is goal for DM pt means that they have well controlled DM. Anything lower - extremely good control and anything over 7%= poor control
Prevention of NIDDM
wt loss, diet, exercise, regular check up with MD
Nutrition therapy goal
maintain BS levels and lipid levels near normal to prevent longterm complication
Components of Diet include a consistent amount of
carbs, proteins, and fats
CCHO diet goal is
less restriction of foods and less rigid; very individualized
Nutritional therapy food plans
limit high fat foods, encourage fruits, veggies, and grains
important to lower cholesterol, BS usually goes down with exercise and insulin requirements decrease.
Insulin needs related to exercise
exercise decreases BS and may decrease insulin needs, at risk for HYPOGLYCEMIA, check BS frequently with change in exercise, DON NOT EXERCISE DURING INSULIN PEAK TIMES
Cautions with exercise
pt taught to carry quick simple sugar source when exercising, AVOID EXERCISE WHEN BS IS GREATER THAN 250 because liver releases glucagon and increases change of diabetic ketoacidosis
blood vessel damage in the eyes; Retinas detach and cause blindness; avoid straining exercise
may injure themselves and not know it; heal slowly or not at all
when pt is NPO for procedure
ask MD if unsure if they want insulin administered; check BS frequently
always given to IDDM; given to NIDDM when ill
sources of insulin
most common is synthetic, also have pork and beef insulin
cultural considerations for insulin
be mindful when giving pork/beef insulin
normal pancreas secretes
1 unit of insulin per hour; secretes more with food intake
precautions for LANTUS/LEVMIR
can not be mixed with other insulin, given only 1 time in 24 hours and does NOT have a peak
Rapid Acting insulin; HumaLOG, NovaLOG
onset 15-30min, peak 30-90min, duration <5 hours
Short acting insulin; Regular; HumuLIN R, NovaLIN R
onset 30-60min, peak 2-5hours, duration 5-8hours
Intermediate Acting; NPH, Humulin N, Novolin N
onset 1 1/2-2hr, peak 4-12 hours, duration 24 hours
Long Acting; Lantus/Levmir
onset 2-4hr, NO PEAK, duration 24hours
humulin 50/50, humulin or novolin 70/30, humalog 75/25
insulin site facts
back of arm, adipose tissue of abdomen, legs, lower back (love handles), shoulder blades; always given SUBQ
closest thing to a pancreas, delivers subQ insulin at a basal rate and allows for bolus administration
benefit for insulin pumps
allows flexibility and a quality of life and reduces the amount of insulin needed
requires close monitoring from an Endocrinologist; pt should know about their condition before running pump
ALWAYS DRAW CLEAR TO CLOUDY
Sliding scales for insulin
dose is based on BS results; not all scales are the same and they are doctor prescribed
occurs related to the release of cortisol early in the morning resulting in high fasting BS results in the am
Procedure for dawn phenomenon
check BS between 2am-4am, high dose of insulin at HS or supper, NPH or Lantus insulin are preferred choices
Oral hypoglycemic agents are given
30 minutes before meal
First generation sulfonylureas;diabinaese, orinase
stimulate insulin release from pancreas; side effects= nausea, anorexia, risk of hypoglycemia; nsg considerations; given BID before breakfast and supper, avoid during pregnancy
Second generation sulfonylureas; amaryl, glucotrol, diabeta, micronase (given to pt's who have higher BS)
stimulates insulin release from pancreas; side effects= N/V, anorexia, risk for hypoglycemia; nsg conisderations= given QD before bfst, do not stop abruptly, avoid during pregnancy
Alpha Glucosidase inhibitors; Precose (used with sulfonylureas)
delays the absorption of CCHO's; side effects=diarrhea, flatulence, hypoglycemia; nsg considerations= given TID before meals, avoid during pregnancy
Biguanide Compounds; Glucophage(meformin)
improves the use of insulin by the body; side effects=N/V/D, hypoglycemia; nsg considerations=avoid alcohol, avoid during pregnancy, MRI precautions (can not take 48 beofre or after and MRI)
Insulin Enhancing Agents; Avandia, Actos
increase the effectiveness of circulating insulin; side effects=liver damage; nsg considerations=liver function test, given QD in the am, avoid during pregnancy
Meglitinides; Prandin, Starlix
stimulates insulin release; side effects= increases risk for infection; nsg considerations= protection for infection, teach s/s of infection and early tx, avoid during prenancy
Self monitoring of Blood Glucose
teach pt importance and how to take bs, take bs before bfst (fasting) and then TID or QID, HGB A1C done every 3-4 months
Goal for Type 2 DM
keep BS 70-110;
Urine glucose and ketone monitoring
check at times of stress or illness, if positive it indicates the bs is really elevated
Ketones in urine
develops when there is no glucose in the cell, body breaks down fat and the waste product is KETONES; check at times of stress and illness
the only cure for diabetes; Immunosuppressants for life which increases risk for infection
occurs when calories exceed insulin available; BS above 200
causes for hyperglycemia
eating too many carbs, not enough insulin, stress and illness
insulin exceeds caloric intake; BS less than 60
causes for hypoglycemia
too much insulin, skipping a meal, exercising during peak times of insulin
S/S of hypoglycemia
h/a, lethargy, diaphoresis, cold, clammy,
DKA= diabetic ketoacidosis
happens in TYPE 1 DM; caused from BS being very HIGH, glucagon released from liver which increases BS even more, EMERGENT SITUATION which will require pt to be in the ICU on an insulin drip. Frequent Accu checks, ABG's to check acidotic status
juicy fruit breath and urine, flushed dry
happens in TYPE 2 DM; results in high BS; still secreting insulin but not enough so no ketones. the increased BS causes the polyuria, glucosuria, dehydration
Nsg for HHNK
monitor BS, insuin, IV fluids for dehydration
prevent long term complications by
maintaining good control of BS
Macrovascular; circulatory system
increased risk for heart disease; MI, CVA, PVD
PVD (peripheral vascular disease)
leads to amputation; S/S= cold extremities, dusky color skin, weak pulse
prevention of heart disease
maintaining good control of BS, exercise, balanced diet, lipid lowering meds
Microvascular; eyes, kidneys
diabetic retinopathy; causes blindness
prevent by seeing a ophthalmologist twice a year and keeping BS and B/P under control
Renal failure- blood vessels in kidney get ruined results in decrease blood supply in kidney; Prevent by BS control, I&O, renal labs to monitor function
unable to feel or sensation of burning/tingling; increased risk for injuries (physical and thermal)
Prevention of foot complications
good BS control, inspect feet (THE WHOLE FOOT) for cracks, dry skin, ingrown toenails, see a podiatrist for any problems and to cut toenails, always wear shoes, no stockings or high heel shoes, wear cotton socks, teach pt the risk of doing foot care on themselves
HIGH AND DRY = INSULIN IS TOO HIGH; s/s extreme thirst, frequent urination, dry skin, hunger, blurred vision, drowsiness, nausea
COLD AND CLAMMY = NEED SOME CANDY; s/s shaking, fast heartbeat, sweating, anxious, dizziness, hunger, impaired vision, weakness, fatigue, headache, irritable
long term affects of DM
heart disease, neuropathy, retinopathy, increased risk for infection, amputation, renal failure
factors that affect the amount of insulin a person takes
diet, stress and illness, exercise, weight, medication, pregnancy
major cause for type 1 DM
autoimmune disorder (THEORIZED.)
when are oral diabetic agents administered
30 min beofre meals
where is insulin given and why
subQ- longer absorption rate
a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization or both
What makes diabetes such a devastating disease?
the long term complications associated with it
Before insulin was discovered, how was diabetes treated?
a diet of salad and eggs
a hormone produced by the beta cells in the islets of Langerhans of the pancreas
How does insulin work (under normal circumstances) to reduce blood glucose levels?
insulin is continuously released into blood stream in small pulsatile increments (basal rate) and increased release (bolus rate) when food is ingested, and works to lower the blood glucose level by working as a "key" to transport sugar from blood stream across the cell membrane to the cytoplasm of the cell, where it can be utilized for energy; stimulates glucose storage in the liver and muscle in the form of glycogen
Under normal circumstances, what is the range that blood glucose levels are maintained at all times?
What is the average amount of insulin secreted daily by an adult under normal circumstances?
hormones that work to oppose the effects of insulin; include glucagon, epinephrine, growth hormone and cortisol
How do counterregulatory hormones prevent a person from becoming hypoglycemic?
they increase blood glucose levels by stimulating glucose production and output by the liver; they also decrease the movement of glucose into the cells
What are the four theories linked to the cause of diabetes mellitus?
genetic, autoimmune, viral, and environmental
Where is glucagon produced?
by the alpha cells in the pancreas
type I diabetes
the end result of a long standing process in which the body's own T cells attack and destroy pancreatic beta cells, which are the source of the body's insulin (autoimmune disease); can also be the result of trauma/disease affecting the pancreas, or an infection that has caused damage to the pancreas; manifests itself when a person can no longer produce insulin; onset of symptoms is usually rapid, but disease process has been ongoing long before symptoms are evident
What are some of the symptoms manifested on onset of diabetes type I?
sudden weight loss, polydipsia, polyuria, polyphagia, weakness/fatigue
a life threatening condition resulting in metabolic acidosis; prevented/treated with administration of an outside source of insulin
the breaking down of glucose
type II diabetes mellitus
most prevealent type of diabetes; occurs when the body cannot use the insulin it makes (receptors have changed so the key/insulin does not work-insulin resistance); can also occur if the insulin produced is not sufficient to decrease the amount of glucose in the blood; can also occure when the liver does not produce enough glucose; gradual onset usually associated with poor eating habits and sedentary lifestyle
Why is type II diabetes now being seen more often in children and adolescents?
this is due to the epidemic of early childhood obesity and the sedentary lifestyles of children
What are some factors that would increase an individuals risk of getting type II diabetes?
genetics (family history); above age 35; obesity (especially abdominal); insulin resistance; high levels of insulin in blood, increased LDL; increased triglycerides; decreased HDL
Which ethnic groups have a higher risk of type II diabetes?
Native Americans, Alaska Natives, African americans, Hispanic Americans, and Asian Americans
diagnosed when fasting glucose levels are higher than normal (100 mg/dl) but lower than 126 mg/dl; people with prediabetes usually develop type II diabetes within 10 years; treat with weight loss and exercise to prevent onset of type II diabetes
develops during pregnancy; will have normal glucose levels within 6 weeks post partum; risk for developing type II diabetes in 5 to 10 years is increased; treated with nutritional therapy and then insulin therapy if that is not sufficient
occurs in some people because of another medical condition or due tot he treatment of a medical condition that causes abnormal blood glucose levels; treated by treating the underlying cause/condition
What three diagnostic tests are used to diagnose diabetes?
fasting plasma glucose level testing, random/casual plasma glucose measurement, and two hour OGTT level testing
fasting plasma glucose level testing
done with no caloric intake for at least eight hours prior; confirmed by repeat testing on another day; preferred method of diagnosis; if glucose level is equal to or greater than 126 on two separate occasions, person is diagnosed with diabetes
random/casual plasma glucose level testing
done anytime of day without regard to the time of the last meal; if glucose level is above 200mg/dl AND the person exhibits manifestations of diabetes ( polyuria, polydipsia, and unexplained weight loss) they are diagnosed with diabetes
two hour OGTT level
accuracy depends on adequate patient preparation and attention to factors that could influence outcome like severe restriction of carbs, acute illness, medications, and restricted activity; if patient has blood glucose levels of above 200 mg/dl they are diagnosed with diabetes
How often should a person over the age of 45 be screened for diabetes?
every 3 years
How often should a person with a BMI of greater than 25 be screened for diabetes?
every 3 years
What are some other circumstances that would require a person under the age of 45 be screened for diabetes every 3 years?
they have a first degree relative with diabetes, they life an inactive lifestyle (bedrest), had a baby weighing over 9 lbs, high cholesterol levels
a test done that shows the amount of glucose attached to hemoblogin molecules over their lifespan (3 months)
What is the recommended hemoglobin A1c percentage for a patient with diabetes?
less than 7 % (some say 6.5%)
What is teh recommended hemoglobin A1c percentage for a patient without diabetes?
Why is the hemoglobin A1c considered the most accurate measurement of glucose control?
Because it loos at the bigger picture (across a 3 month span)
What should be included in the eduation of a diabetic patient?
medication, food intake (also teach person preparing patient's meals), exercise, blood glucose testing
used to control postmeal blood glucose levels; onset is 15 minutes; peak is 60-90 minutes; duration is 3-4 hours; include lispro, aspart, and glulisine
used to control postmeal blood glucose levels; onset is 1/2-1 hr; peak is 2-3 hrs; duration is 3-6 hrs; regular insulin
How long before a meal should rapid-acting insulin be injected?
How long before a meal should short-acting insulin be injected?
making more glucose
used in combination therapy to control blood glucose levels between meal times and overnight; can be mixed with short or rapid acting insulin to avoid more injections; more appealing to patient than long acting (which can not be mixed with short/rapid acting in the same injection) but may not achieve sufficient blood glucose control; onset time is 2-4 hrs; peak is 4-10 hrs; duration 10-16 hrs; NPH insulin
very long-acting insulin
used in addition to bolus insulin, but can not be mixed in same syringe; controls glucose levels between mealtimes and overnight; onset is 1-2 hrs; no pronounced peak; duration is 24+ hrs; glargine and detemir; can not prefill syringes with glargine, must be filled right before administration
premixed by the manufacture; 70/30 NPH/regular (composed of 70% NPH and 30% regular); 50/50 nph/regular; 75/25 lispro protamine/lispro; 70/30 aspart protamine/aspart
What is the goal of insulin therapy?
to mimic normal pancreatic insulin production
What is the key to successful blood glucose control?
self blood glucose monitoring
What should a nurse ALWAYS do before administering insulin?
check the vial and dosage with another nurse while needle is still in syringe
used to control glucose levels between meals and overnight; onset is 30min-3 hrs; peak is 10-20 hrs; duration is up to 36 hrs; ultralente insulin
How does sliding scale administration work?
a predetermined amount of insulin to be administered is based on the blood glucose level of the patient at that time
What should be included in the education of the patient about insulin administration?
wash hands and inspect vial; gently roll the vial to mix suspensions; rotate sites within one anatomical area (to keep absorption rate more consistent between administrations); store prefilled syringes for up to 30 days with needles pointing up; can store unopened vials at room temperature for up to 4 weeks
Can insulin be taken orally?
no because it is a protein and the digestive enzymes would denature it
intensive insulin therapy
insulin therapy that requires multiple daily injections of insulin and frequent self monitoring of blood glucose levels (4-6 times per day)
Which type of insulin can be given IV?
regular insulin when immediate onset is desired
If a patient is given 70/30 NPH/regular insulin at 7am, when are they most likely to have a hypoglycemic episode?
between 4 and 6 pm
What are some problems sometimes seen with insulin therapy?
hypoglycemia; allergic reaction to insulin; lipodystrophy; somogyi effect; dawn phenomenon
allergic reactions to insulin
local inflammatory reaction to insulin injection site; itching, erythema, and burning; may be self limiting within 1-3 months or may be treated with a low dose of antihistamine; true allergic reaction is rare and more often associated with preservatives used and in the latex stoppers on the vials rather than in the insulin itself
atrophy of subcutaneous tissue and may occur if hte same injection site is used too frequently; prevented by rotation of injection sites
hardening of the subcutaneous tissue associated with lipodystrophy, regresses if patient does not use site for at least six months; can cause decreased absorption of insulin administered
nightime hypoglycemia caused by insulin overdose; counterregulatory hormones cause high blood sugar in the am; can result in patient or provider increasing insulin dosage in the morning, causing more hypoglycemic effect; treated by decreasing insulin dosage given at night
counterregulatory hormones secreted during sleep cause high am blood sugar; glowth hormones and cortisol play a role in this phenomenon; treated by patient eating a snack before bedtime to keep blood sugar from dropping overnight
not insulin; work to improve the mechanisms by which insulin and glucose are produced and used in the body; used to treat type II diabetes
drug of choice for treating type II because of the decreased chance of prolonged hypoglycemia; increases insulin production from the pancreas; 10% of patiets experience decreased effectiveness
increases insulin production from the pancreas; more rapidly absorbed and eliminated than sulfonylureas; should be taken anytime from 30 minutes before meal; should NOT be taken is meal is skipped
help insulin's action at the receptor site on the cell membrane and reduces glucose production by the liver; does not promote weight gain
alpha glucosidase inhibitors
aka "starch blockers"; work by slowing down the absorption of carbohydrates in the small intestines; taken with the first bite of each meal
most effective in those with insulin resistenance; improves insulin sensitivity, transport, and utilization at target tissues; can cause edema-not to be used in patients with CHF
dipeptidyl peptidase-4 inhibitors (DPP4's)
work by increasing and prolonging incretin levels; responds to elevated glucose levels; lowers glucose production by the liver; lower potential for hypoglycemia than some agents
a hormone produced by the intestine which increases insulin synthesis and release from the pancreas
What class of drugs are glipizide and glimepiride in?
What class of drugs are repaglinic and nateglinide in?
What class of drugs is metformin in?
What class of drugs is acarbose in?
alpha glucosidase inhibitors
What class of drugs are pioglitazone and rosiglitazone in?
What are the three drugs combined with metformin in combination therapy tablets?
glyburide, rosiglitazone and glipizide
What must you remember about metformin?
can not be given for 48 hours after IV contrast has been given or 24 hours prior
What is the most important thing to remember about nutritional therapy for a type I diabetic patient
CONSISTENCY in timing and amount of food because of the insulin therapy
What is important to emphasize when education a type II diabetic patient about nutritional therapy?
glucose, lipid and blood pressure goals as well as carlorie/fat reduction
What is the plate method?
1/2 non starchy veggie; 1/4 starchy veggie; 1-4 protein; glass of nonfat milk; 1 serving of fresh fruit
term used to describe the rise in blood glucose after a person has consumed a carbohydrate
What is involved in patient teaching surrounding exercise?
should be consistent; should check blood glucose before during and after (especially if starting a new program); increase insulin receptor sights and have a direct effect on lowering blood glucose and weight loss; best scheduled 1 hour after meal; keep snacks available every 30 minutes during exercise; delay or modify exercise if BG is above 250
What is involved in patient teaching surrounding self blood glucose monitoring?
keep a dated written record; adjust treatment regimen to obtain optimal control; check 2-3 times/day; before meals bedtime and anytime if hypoglycemia is suspected
glucose urine testing
not accurate due to renal threshold
ketones in urine
signals risk for ketoacidosis; by product of fat breakdown in the absence of insulin; test for ketones when blood glucose level is over 240 for two tests, illness, diabetic or pregnant
What should I do if I'm sick and diabetic?
continue regular meal plan; increase noncaloric fluids and decaffeinated beverages; continue oral agents and insulin as prescribed; check glucose every 4 hours
diabetic ketoacidosis diagnostics
blood pH less than 7.3; decreased bicarbonate level; ketones present in urine
What symptoms are related to the fluid shift resulting from osomotic effects of high blood glucose?
polydipsia and polyuria
What are the signs and symptoms of DKA?
polyuria, polydipsia, polyphagia, lethargy, coma, dehydration, acidosis, acetone breath, kussmaul's respirations
How is DKA treated and managed?
ABC's first; rehydration with saline until output is 30-60ml per hour; restore electrolytes; give insulin (after saline); give sodium bicarbonate if blood pH is less than 7.3
hyperosmolar hyperglycemic syndrome
seen in type II diabetes; enough insulin produced to prevent DKA, but sever hyperglycemia, osmotic diuresis and extracellular fluid depletion is needed; treated as a medical emergency with high mortality rate; treated similar to DKA
What are the signs and symptoms of hyperosmolar hyperglycemic syndrome?
very high blood glucose levels; marked increase in serum osmolality; impaired thirst or inability to replace fluids; neurological changes; hypotension; dehydration; tachycardia; ketone bodies absent or minimal
low blood glucose; occurs when there is not enough food intake, too much insulin, or too much exercise; characterized by a blood glucose level of less than 70
What are the signs and symptoms of hypoglycemia?
confusion, irritability, sweating, tremors, weakness, visual disturbances, unconsciousness, seizures, coma and death
How is hypoglycemia treated?
check blood glucose; immediately ingest 15-20 gm of a simple carb; 4-6 oz of oj, soft drink, 8oz of milk; avoid fat containing sweets (take longer to absorb); recheck blood glucose in 45 min.; may be treated with 20-50 ml of 50% dextrose IV push
diseases of the large and medium size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes; atherosclerosis; increased risk of heart attack, stroke and amputations
How can macrovascular complications be prevented?
by not smoking, controlling hypertension, decreasing fat intake, losing weight and being active
result from the thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia; specific to diabetes
the process of microvascular damage to the retina as a result of chronic hyperglycemia in patients with diabetes
non proliferative retinopathy
most common form of retinopathy; partial occlusion of the small blood vessels in the retina causes the development of microaneurysms in teh capillary walls
the most severe form; involves the retina and vitreous; when retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood; these new blood vessels are fragile and hemorrhage easily
a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney; kidney's filtration mechanism is stressed, holes and fibrous tissue develop; protein leaks out into urine
nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus
loss of sensation; pain; abnormal sensation; complete or partial loss of sensitivity to touch and temperature is common; can cause atrophy of the small muscles of the hands and feet
What is the treatment for sensory neuropathy?
control of blood glucose, pain medications, capsaicin, tricyclic antidepressants
affects nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence, and diarrhea/urinary retention
can cause nausea, vomiting, reflux and delayed absorption of food, hypoglycemia (can't tell they are hungry/ don't eat)
What is the most common cause of hospitalization of people with diabetes?
What are some risk factors for developing foot complications?
sensory neuropathy; peripheral arterial disease, clotting abnormalities, impaire immune function, autonomic neuropathy, smoking, improper footwear, going barefoot
How are foot complications prevented?
prescription footwear; diligent skin and nail care; inspect foot thoroughly each day; treat small problems promptly
Why are diabetic people more susceptible to infection?
decreased circulation leads to a defect in the mobilization of inflammatory cells; impaired phagocytosis; neuropathy delays detection
Why does prevalence of diabetes increase with age?
reduction of beta cell function; decreased insulin sensitivity; altered metabolism of carbohydrates; likely to be recieving medications that can impair action of insulin