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164 Cards in this Set

  • Front
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What is diabetes?
diabetes is a chronic multi system disease related to ABNORMAL INSULIN PRODUCTION; OR IMPAIRED INSULIN UNTILIZATION; OR BOTH
DM is the leading cause of?
1. end stage renal disease (kidney disease)
2. adult blindness
3. non traumatic lower limb amputations
DM is a major contributing factor to:
1. Heart disease (2x higher than people w/o diabetes)
2. stroke (2-4x higher w/ people w/ diabetes)
What is the etiology and pathophysiology of diabetes?
It is primarily a disorder of glucose metabolism related to absent or insufficient insulin supplies and/or poor utilization of insulin that is available
What is insulin?
a hormone
where is insulin produced?
insulin is produced in the B cells in the ISLETS OF LANGERHANS OF THE PANCREAS
What does insulin do?
controls the level of glucose in the blood by regulating the production and storage of glucose
How is normal insulin released?
normal insulin is released continuously into the bloodstream at a basal rate with increased release (bolus) when food is ingested (prandial)
During a fasting state, a stable and normal glucose range is...
70-120 mg/dl
The average daily amount of insulin secreted by an adult is..
40-50 mg/dl
when a person eats a meal, insulin secretion increases moving from the _____ --> _____ --> _____ --> ______
when a person eats a mean insulin secretion increase moving from the blood, to muscle, to liver, to adipose tissue (fat cells)
What do counterregulatory hormones do?
they oppose the effects of insulin, increase blood glucose levels (stimulate glucose production and output), with insulin: profile a regulated release of glucose for energy, and, help maintain normal blood glucose levels within range
Name 4 counterregulatory hormones..
glucagon, epinephrine, growth hormone, cortisol
what is gluconeogenesis?
formation of glucose, amino acids and fats
there is a decrease in insulin production when?
during overnight fasting
An absence of insulin prevents some cells from using _______ for ______
an absence of insulin prevents some cells from using glucose for energy
During an absence of insulin, counter regulatory hormone levels _______ in attempt to make glucose from other sources
During an absence of insulin, counter regulatory hormone levels increase in attempt to make glucose from other sources
an absence of insulin leads to __________
absence of insulin leads to HYPERGLYCEMIA
- F/E imbalances, classic s/s DM
During an absence of insulin, there is a buildup of ketones which leads to ?
a buildup of ketones leads to metabolic acidosis
during an absence of insulin, dehydration occurs, which leads to?
hemoconcentration, hypovolemia, hyperviscosity (thick coagulated blood), hypoperusion or hypoxia
During an insulin deficiency, fats break down into free fatty acids, they float around in the blood and cause _________
metabolic acidosis ... which is a build up of ketones (ketonuria)
The classic cardinal signs of DM are?
Polyphagia (extreme hunger), polyuria (excessive production of urine), polydyspia (extreme thirst)
If there is a drop in glucose level, what happens?
insulin secretion stops, and glucagon is released
what does glucagon do?
releases glucose from liver
how is liver glucose made?
made via glycogenolysis and gluconeogenesis
glucoeneogensis is?
glucose into glycogen
risk factors for developing DM?
1. family hx (parents or siblings with DM or 1st degree relatives
2. obesity: BMI > 25%
3. sedentary lifestyle
4. certain race and ethnicities
5. age: >45
6. A1C >5.7 or IFG on previous testing
7. Hypertensive: >140/90 or on therapy
8. HDL cholesterol <35 mg/dl & or triglycerides level > 250 mg/dL
9. history gestational diabetes or delivery of baby over lbs
10. history of vascular disease
11. have polycystic ovary syndrome
There are 4 methods to diagnose DM..they are..
1. A1C test
2. Fasting plasma glucose level
3. random or casual plasma glucose measurement
4. two-hour OGTT level test
To diagnose DM, an A1C level would be..
A1C greater or equal to 6.5%
To diagnose DM, a fasting plasma glucose level would be..
fasting plasma glucose level greater than 126 mg/dL ((mud be choloric free for 8 hours))
During an insulin deficiency, fats break down into free fatty acids, they float around in the blood and cause _________
metabolic acidosis ... which is a build up of ketones (ketonuria)
The classic cardinal signs of DM are?
Polyphagia (extreme hunger), polyuria (excessive production of urine), polydyspia (extreme thirst)
If there is a drop in glucose level, what happens?
insulin secretion stops, and glucagon is released
what does glucagon do?
releases glucose from liver
how is liver glucose made?
made via glycogenolysis and gluconeogenesis
glucoeneogensis is?
glucose into glycogen
risk factors for developing DM?
1. family hx (parents or siblings with DM or 1st degree relatives
2. obesity: BMI > 25%
3. sedentary lifestyle
4. certain race and ethnicities
5. age: >45
6. A1C >5.7 or IFG on previous testing
7. Hypertensive: >140/90 or on therapy
8. HDL cholesterol <35 mg/dl & or triglycerides level > 250 mg/dL
9. history gestational diabetes or delivery of baby over lbs
10. history of vascular disease
11. have polycystic ovary syndrome
There are 4 methods to diagnose DM..they are..
1. A1C test
2. Fasting plasma glucose level
3. random or casual plasma glucose measurement
4. two-hour OGTT level test
To diagnose DM, an A1C level would be..
A1C greater or equal to 6.5%
To diagnose DM, a fasting plasma glucose level would be..
fasting plasma glucose level greater than 126 mg/dL ((must be choloric free for 8 hours)) ((on 2 occasions to confirm DM))
To diagnose DM, a random or casual plasma glucose measurement would be..
Random or casual plasma glucose measurement greater or equal to 200 mg/dL plus symptoms ((casual can be taken any time of day w/o regards to last meal))
To diagnose DM, a two-hour OGTT level must me..
two-hour OGTT level greater or equal to 200 mg/dl when a glucose load of 75 g is used
((glucose load is syrupy and sweet))
Pre diabetes is characterized by what two test?
IFG (impaired fasting glucose) and IGT (impaired glucose tolerance)
What levels for an IFG would indicate pre diabetes?
IFG
-blood glucose levels are >100 mg/dl but <125 mg/dl when fasting
- high risk for type 2 DM
What levels for an IGT would indicate pre diabetes?
IGT
- 2 hour plasma oral glucose test (OGTT) higher than normal (between 140 - 199mg/dl)
Type 1 DM: also known as:
juvenile onset, insulin dependent, IDDM, brittle diabetic
Type 1 DM: age of onset:
any age, most commonly seen in people under 40 years of age
Type 1 DM: peak of onset:
between ages 11-13
Type 1 DM: type of onset:
abrupt w/ classic s/s
Type 1 DM: nutritional status:
nonobese; seen in people with a lean body, can occur in the over wt. but rare
Type 1 DM: primary defect:
absent or minimal production of insulin
Type 1 DM: islet cell antibodies:
often present at onset
Type 1 DM: endogenous insulin:
minimal or abset
Type 1 DM: symptoms:
class 3P's (polydyspia, polyphagia, polyuria), fatigue, wt. loss
Type 1 DM: ketosis:
prone at onset or during insulin deficiency
Type 1 DM: nutritional therapy:
essential
Type 1 DM: insulin?
required for all
Type 1 DM: vascular and neurologic complications?
frequent
Type 1 DM: Etiology and pathophysiology of DM:
destruction of pancreatic beta cells due to an autoimmune process ((produces little or no insulin)) (( progressive destruction of pancreas))
Destruction of beta cells result in:
1. decrease insulin production
2. uncheck glucose production by liver
3. fasting hyperglycemia
4. postprandial(After meals) hyperglycemia
5. glycosuria which leads to osmotic diuresis
6. ketones prone when in absence of insulin
Type 1 DM: onset of disease:
onset of disease:
-long preclinical period
-longstanding presence of islet cell antibodies
-manifestations develop when pancreas can no longer produce insulin
-rapid onset of symptoms
-present at ED with impending or ketoacidosis
-classic symptoms: 3 P's
- sudden and recent wt. loss
Type 1 DM: will require _____ to survive
exogenous insulin to sustain life
Type 1 DM: onset of disease, DKA is commonly seem during onset....DKA occurs why and when?
-occurs in absence of exogenous insulin
-life-thretening condition
-results in metabolic acidosis
Type 2 DM: prevalence:
most prevalent type: 90-95% of all DM
Type 2 DM: formerly known as..
adult onset or NIDDM
Type 2 DM: primary defect?
insulin resistance and impaired insulin secretion
Type 2 DM: age at onset:
any age, usually over 30
Type 2 DM: type of onset:
insidious, may go undetected for years
Type 2 DM: environmental:
obesity: 80-90% are overweight at diagnosis lack of excerise
Type 2 DM: islet cell antibodies:
absent
Type 2 DM: endogenous insulin:
possible excessive, adequate or delayed secretion or reduced utilization; diminishes over time
Type 2 DM: nutritional status:
obese or normal
Type 2 DM: symptoms:
none or presence of classic
Type 2 DM: ketones:
resistant except during periods of infection or stress
Type 2 DM: nutritional therapy:
essential
Type 2 DM: insulin needed?
no; but may require on short term or long term basis to prevent hypoglycemia or during periods of stress or infection
Type 2 DM: vascular and neurologic problems?
frequent
Type 2 DM: HHNS (hyperosmolar):
no ketones are produced by uncontrolled type 2 DM
Type 2 DM: etiology and pathophysiology:
-pancreas continues to produce some endogenous insulin
-impaired insulin secretion: characteristic of type 2
-not enough insulin, or the insulin they have does not work properly at the cellular level (insulin resistance)
Type 2 DM: obesity seen where?
abdominal and visceral
-obesity is most powerful risk factor
-associated with INSULIN RESISTANCE
-DIET AND EXERCISE (ENHANCES EFFECTIVENESS OR INSULIN)
Type 2 DM: etiology and pathophysiology: Four major metabolic abnormalities:
1. insulin resistance
2. pancreas decrease ability to produce insulin
3. inappropriate glucose production from liver
4. alteration in production of hormones and adipokines
-adiponection and leptin (effect insulin sensitivity)
Metabolic Syndrome: is what?
Metabolic Syndrome is a cluster of abnormalities that act synergistically to greatly increase the risk for cardiovascular disease and diabetes
Metabolic Syndrome: is characterized by:
-insulin resistance
-elevated insulin levels
-high levels of triglycerides
-decreased levels of HDLs
-increased levels of LDLs
-hypertension
Metabolic Syndrome: how is it diagnosed?
to confirm Metabolic Syndrome, there must of 3 or more of the following present:
- men --> equal to or greater than 40 inches
-women --> equal or greater than 35 inches
-elevated triglycerides: equal to or greater than 150 mg/dl
-reduced HDL (good) cholesterol:
-men less than 40mg/dl
-women less than 50 mg/dl
-Elevated blood pressure: equal to or greater than 130/85 mm Hg
-Elevated fasting glucose: equal to or greater than 100 mg/dl
Metabolic Syndrome:(syndrome X) you'll see:
central obesity, high BP, high triglycerides, low HDL cholesterol, insulin resistance
Type 2 DM:
-gradual onset
-person may go years with undetected hyperglycemia
-osmotic F&E loss from hyperglycemia may become severe
-hyperosmolar coma
Clinical manifestations for type 1 DM:
-Classic S/S: 3Ps
-Weight loss
-weakness
-fatigue
Clinical manifestations for type 2 DM:
-Nonspecific symptoms
-may have classic s/s
-fatigue
-recurrent infection
-recurrent vaginal years or monili infection (vagina itching)
-prolonged wound healing
-visual changes
DM: Diagnostic Studies: Hemoglobin A1C test:
-useful in determining glycemic levels over time
0shows the amount of glucose attached to hemoglobin molecules over RBC life span(120 days)
-A1c > 6.5% confirms DM
Normal A1C level is:
4-6%
What is the monofilamaent test?
it is a neurological exam that tests for neuropathy....by measuring sensation in feet
How to test for ketones:
URINE DIPSTICK (detects ketonuria)
-reagent pad on strip turns purple when ketones present
-should be done with type 1 w/ glycosuria or persistently high glucose levels: >240 mg/dl and during illness, in pregnancy w/ preexisting DM and in gestational DM
3 types of rapid acting insulin used:
Humalog, Novolog, Apidra
Rapid acting insulin: onset:
5-15 minutes
Rapid acting insulin: peak:
1-2 hours
Rapid acting insulin: duration:
2-4 hours
Rapid acting insulin: also known as:
meal time insulin
Rapid acting insulin: solution color?
clear
Rapid acting insulin: when do you inject?
0-15 minutes before meal (((must have tray available)))
with rapid acting insulin, pt will also require a _______
long acting insulin
Rapid acting insulin: helps control:
post meal hyperglycemia
look for hypoglycemia during what time?
peak time!
If pt. is hyperosmolar or in DKA...give?
short acting regular insulin via IV
how do you mix insulin??
clear to cloudy
Regular insulin (short acting): solution color?
clear
Regular insulin (short acting): onset:
30 minutes - 1 hour
Regular insulin (short acting): peak:
2-3 hours
Regular insulin (short acting): duration:
3-6 hours
Regular insulin (short acting): inject when?
30-45 minutes before mean, to make sure onset of action coincides with meal absoription
Regular insulin (short acting): types or Regular insulin....
Humilin R or Novolin R
NPH Intermediate Acting Insulin: onset:
2-4 hours
NPH Intermediate Acting Insulin: peak:
4-12 hours
NPH Intermediate Acting Insulin: Duration:
10-16 hours
NPH Intermediate Acting Insulin: color of solution?
cloudy
NPH Intermediate Acting Insulin: is ordered as?
pre-deinner insulin, also used at bedtime...important that patient has a snack...tends to peak laster in the afternoon if given in a.m....pre-dinner (5pm) peaks anytime after midnight
Give patient NPH at 7am, you can start to see it peak at 11 am, and max peak at?
2 pm NPH peaks 4-12 hours
Gave patient 45 units NPH at 7am, when can nurse expect to see hypoglycemic episode?
2 pm! NPH peaks 4-12 hours
What do you do if you see hypoglycemia?
give a snack!
Long acting insulin: onset:
1 hour
Long acting insulin: peak:
peakless
Long acting insulin: duration:
24 hours
Because Long acting insulins are peakless, risk for hypoglycemia is...
greatly reduced
2 Long acting insulins are:
Lantus and Levemir
Long acting insulin is also known as a basal dose:
basal rate is the amount of insulin required to manage normal daily glucose fluculations
Long acting insulin: administer how many times a day?
1 hour
Long acting insulin: what color insulin?
clear
Long acting insulin: can it be mixed?
can't dilute or mix with any other insulin or solution
Long acting insulin: is released:
steadily and continuously
Long acting insulin: give when and how?
give bedtime or a.m as a subq injection
What is combination therapy?
-different insulins premixed together
-for those who do not want to use more than one or two injections per day
-may not achieve the kind of blood glucose control that can be achieved with basal-bolus therapy
Insulin administration: when do you use IV and which insulin can be given IV?
Administer regular insulin via IV during DKA or hyperosmoloar
Fastest site of insulin absorption?
abdomen: fasted absorption, followed by arm, thigh and buttock
Don't inject in site that are:
swelling, have dressings, or anything that might prevent absorption...don't inject in areas that are about to be exercised, this may speed up absorption and increase peak/onset timing
What is the somogyi effect?
-rebound effect in which an overdose of insulin induces hypoglycemia
-nocturnal hypoglycemia followed by a rebound hyperglycemia (pre breakfast)
When does somogyi effect usually occur?
during the hours of sleep, producing a decline in blood sugar in response to too much insulin
somogyi effect:rebound hyperglycemia and ketones occurs as a result of:
rebound hyperglycemia and ketones occurs as a result of counterregulatory hormones being released and stimulating lipolysis, gluconeogenesis and glycogenolysis
Somogyi effect is associated with:
associated with the occurrence of undetected hypoglycemia during sleep, although it can happen at anytime
If somogyi effect is suspected as a cause of early morning high blood glucose levels, the pt. may be advised to:
check blood glucose levels b/w 2 am and 4 am to determine if hypoglycemia is present at the time [ if it is, insulin dosage affecting early morning blood glucose is reduced ]
If somogyi effect is present:
decrease evening (pre dinner) or bedtime dose of intermediate acting insulin or increase food intake (bedtime snack)
Dawn phenomenon:
hyperglycemia that is present on awakening in the morning due to release of counterregulatory hormones (growth hormone and cortisol) in pre dawn hours
Somogyi clues vs dawn clues
SOmogyi clues:
-SO much insulin given
previous night
-Treatment: decrease insulin
dose previous night

Dawn clues:
-DOWN insulin (less insulin)
-- Treatment: INCREASE insulin dose previous night


*both are due to action of counterregulatory hormones acting up
*both result in pre-breakfast hyperglycemia
How does exercise help DM?
it increases insulin receptor sites
-skeletal muscle and adipose tissue have specific insulin receptors
How to exercise safety with DM:
exercise 1 hour after meal, or after 10-15 g carb snack, and check glucose before exercise
When is pancreas transplantation and option?
done for pt. with end stage renal disease and for patients who had or plan to have a kidney transplant
Herbs that lover blood glucose:
aloe vera, bilberry, bitter melon, fenugreek, fish oils, garlic, ginseng, gymna (milk thistle, noapl)
Herbs that increase sugar:
celery seed, rosemary, melatonin
Diabetic ketoacidosis (DKA) is also known as:
diabetic acidosis or diabetic coma
Diabetic ketoacidosis (DKA) is caused by:
a profound deficiency of insulin
Diabetic ketoacidosis (DKA) is characterized by:
hyperglycemia, ketosis, acidosis, dehydration
Diabetic ketoacidosis (DKA) most commonly occurs in:
type 1 DM
Precipitating factors of Diabetic ketoacidosis (DKA) are:
illness, infection, inadequate insulin dosage, undiagnosed type 1, poor self-management, neglect
Diabetic ketoacidosis (DKA) can be seen in type 2 DM when?
during severe illness/stress, when pancreas cannon meet extra demands for insulin
During Diabetic ketoacidosis (DKA)...counterregulatory hormones are...
conterregulatory hormones are increasing, which causes and increase production of glucose
Pathophysiology of Diabetic ketoacidosis (DKA):
Insufficient supply of insulin
-glucose cannot be properly used for energy
-body breaks down fat stores
-ketones are by-products of fat metabolism
-alters pH balance, causing metabolic acidosis (high anion gap acidosis)
-ketone bodies excreted in urine (ketonuria)
-electrolytes become depleted
-Na, K, Cl, Mg, Ph
During Diabetic ketoacidosis (DKA), most important to watch for:
hypokalemia and hyperkalemia
Commonly seen with Diabetic ketoacidosis (DKA):
-vomitting (acidosis and F/E losses)
-hypovolemia followed by shock
-renal failure secondary to hypovolemia and shock
-coma (untreated): dehydration and electrolyte depletion and acidosis
-death (no treatment)
main factors of Diabetic ketoacidosis (DKA) are:
1. decreased or missed dose of insulin
2. illness or infection
3. undiagnosed and untreated diabetes (DKA make be the initial manifestation of diabetes)
4. change in diet, insulin or exercise regimen
Clinical manifestations for Diabetic ketoacidosis (DKA):
-dehydration
-lethargy and weakness: early symptoms
-abdominal pain w/ V/V
- weak, rapid pulse
-KUSSMAULS RESPIRATIONS
-SWEET, FRUITY BREATH ODOR (ACETONE)
Diabetic ketoacidosis (DKA) LAB findings:
-elevated blood glucose level above 250 mg/dl
-ABG: ph < 7.30, HCO3 < 15 mEq/L
-Ketones: urine and blood
-Na, K: low, normal or high: depending on amount of water loss (dehydration)
- Creat/BUN, Hct: elevation: seen w/ dehydration
Collaborative management for Diabetic ketoacidosis (DKA):
Correct f/e imbalance
-IV infusion 0.45% or 0.9% NaCl
-restore urine output (30-60 ml/hr)
-raise blood pressure
-When blood glucose levels approach 250 mg/dl
-SWITCH THE BAG
-5% dextrose added to regimen
-prevent hypoglycemia
-Potassium replacement: treat HYPOKALEMIA
-Sodium bicarbonate: only if pH < 7.0
Diabetic ketoacidosis (DKA) collaborative management:
-Aim F/E: replace ECF & ICF water, correct deficits
- Cardiac or renal compromise: monitor for FLUID OVERLOAD
-Serum K: obtain prior to insulin administration
-blood glucose levels
Diabetic ketoacidosis (DKA) collaborative management and insulin therapy:
Insulin therapy
-to correct hyperglycemia and hyperketonuria
-WITHHELD UNTIL FLUID RESUSCITATION AND K LEVEL IS > 3.5 mEq/L
-BOLUS INSULIN AS ORDERED
-START CONTINUOUS DRIP AT 0.1 UNITS/KG/HR (PUMP)
-lower glucose gradually to avoid cerebral edema
-lower blood sugar by 36-54 mg/dl per hours
Safety alert for DKA and treatment::
too rapid administration of IV fluids and a rapid lowering or serum glucose will lead to CEREBRAL EDEMA
What to do for DKA:
-Administer IVF
-IV administration: regular insulin
-E-lyte replacement
-I&O
-Mental status assessment
-CVP if indicated (central venous pressure)
-Blood glucose assessment
-EKG monitoring
-CV and respiratory assessment