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diabetes

QuestionAnswer
Type 1 diabtes 3-p's, thin and underweight, fatigue and malaise and has abrupt onset
Type II non-insulin dependent, gradual onset, adults over 30 years old
Three abnormalities of Type II Insulin resistance, Abnormal insulin production, gluconeogenisis
what is insulin resistance Increase BS, even with increased level of insulin; poor utilization of insulin at the cell level
Abnormal insulin production Hyperinsulinemia, decreased insulin production
Hyperinsulinemia Occurs in early stages of Type II, High levels of insulin levels in blood. Beta cells work overtime to make up insulin resistance problems.
Decreased insulin production Later stage when beta cells tire and can't keep up and increase demand as BS increases.
gluconeogenesis production of glucose from the liver even though BS is increased already
Risk factors of Type II obesity, BMI greater than 27, truncal obesity (apple shape) physical inactivity.
polycystic ovarian syndrome High risk factor between this and insulin resistance.
acanthosis nigricans brown hyperpigmented thickening of the skin- more common in AA, hispanic
this sign & sx is associated with high levels of circulating insulin and insulin resistance acanthosis nigricans
s/sx of children with type II acanthosis nigricans, dyslipidemia, polycystic ovary syndrome.
what is the best course of treatment for children with type II? wt reduction can cure the disease
Metformin can be used in kids at what age 10
Pre-diabetes Impaired glucose tolerance; impaired fasting glucose
fasting glucose for pre-diabetes > 100 and < 126
Pre-diabtes test when given 75 mg of glucose you are pre-diabetes if glucose level > 140 and < 200
Insulin resistance with mild alteration in beta cell formation pre-diabetes
If someone has pre-diabetes, then what are the chances of it turning to Type II? 1 in 4 chances of becoming diabetec
what is a substantial risk of pre-diabetes? cardiovascular disease
metabolic syndrome insulin resistance syndrome and syndrome X
known as the silent killer metabolic syndrome
Metabolic syndrome is considered a ________________ to DM and cardio vascular disease pre-cursor
A chronic low grade inflammatory process leading to plaque formation in vessels define metabolic syndrome
Hypeinsulinemia high insulin levels in blood...beta cells work overtime to make up for insulin resistance problem.
Uncontrolled htn leads to what? plaque formation in the vessels
Hypertriglyceridemia abnormal number of tryiglycerides that is correlated to plaque for mation.
Low levels of HDL and changes in LDL is another symptom of Metabolic syndrome
visceral adiposity apple shape (abdominal obesity) is another condition that are symptoms of metabolic syndrome
Polycystic ovarian syndrome cysts on ovarians r/t insulin resistance
At risk for developing Type II if you have this condition metabolic syndrome
There are 7 symptoms of metabolic syndrome Hyperinsulinemia, HTN, Hypertriglyceridemia, Low levels of HDL and change in LDL, ab obesity (viseral adiposity), and polycystic ovarian syndrome
type 1 1/2 or 1.5 Latent autoimmune diabetes in adults (LADA)
Type 1 diabetes that occurs over a long period of time and shows up over 30 yrs of age type 1.5 dm
S. sx of type 1.5 dm Pt not overwt, does not have insulin resistance.
antibodies killing of cells in pancreas causing it to eventually shut down. Type 1.5 dm
How is DM II diagnosed? when Fasting BG is >126 x 2 readings & random glucose is > 200
what other symptoms of DM II diagnosis besides FBG & random glucose the 3 p's, unexpected wt loss, blurred vision and presence of ketones
What is the two hour BS test another test to see if you have DM II, you are given 75g of glucose and positive result if bs > 200
secondary diabetes is caused by disease diabetes developed secondary to other condition such as pancreatitis, pancreatic cancer, and cystic fibrosis
secondary diabetes is caused by which medication? treatment of corticosteroids
Gestational diabetes Pregnancey dm
what leads to chubby baby's? maternal blood to the fetus results in increased BS
Is there a risk for someone with gestational dm to get type II? Yes...there is a risk that it could show up 5 to 10 years later.
Does baby born of gestational dm mother have risk of developing dm? Yes, there is a risk
The difference between Type 1 & 2 DM Type 1 can't be Prevented, Type II can be prevented (for the most part)
Obesity is a major factor of Type II because decreases beta cell response to hyperglycemia, leads to insulin receptor abnormalites, and insulin resistance
water follows salt and something else glucose
Increase of glucose draws what? it draws water to it and increases osmoality so that water can't reabsorb into the body.
Where glucose goes water follows and increases the osmoality so that water can't reabsorb into body.
hypoglycemia Blood glucose is less than 60
what things decrease bs? etoh, overexertion, limited food intake, too much insulin, gastroparesis (food just sits in gut and can't be absorbed into body)
why would you have hunger, diaphoresis, weakness, nervousness, shaking, HA and apprehension with Hypogylcemia? Because low glucose = low energy....your hungry cuz your body needs glucose for energy...low BS means dehydration so the other symptoms are of dehydration.
Later stages of hypoglycemia are mental status changes
confusion, slurred speech, somnolence (sleepy) staring, stupor, seizures, or coma later stages of hypoglycemia
What blocks symptoms of hypoglycemia? beta blockers
what happens if hypoglycemia occurs during the night? bizarre nightmares, restless/sleepless, difficult to arouse, and confusion
somogyi effects type 1 or type II type I
Dawn phenom effects type I or Type II? Type II
Which phenom/effect of night hypoglycemia responsd with the release of stress hormones? Somogyi effect or rebound
Which phenom/effect of night hypoglycemia responds with gluconeogenesis? Dawn phenom
gluconeogenesis a type II defect where stored glycogen is converted to glucose via the liver and causes and increase of BS.
what effect occurs as a result of insulin resistance? The pancreas spits out a ton of insulin,that body can't utilize, in response to increase insulin, gluconeogensis occurs...but insulin still can't work with the extra BS, resulting in increase BS
DKA Occurs with type 1 as a result out of control BS or undiagnosed type 1
There is no insulin to breakdown excess glucose for energy, the next option is to breakdown fat for energy and they by-product is ketones and leads to metabolic acidosis DKA
no insulin to convert glucose to energy results in high BS
Type 1 has no insulin to convert out of control BS to energy, where does body go next for energy it breaksdown fat and converts to energy...it is short lived and a by-product of it is ketones
Is DKA gradual or sudden onset? both
Some early symptoms of DKA BS > 250 & as high as 800; 3 p's, dehydration symptoms, hypokalemia, FRUITY BREATH, metabolic acidosis, tachycardia
Why such dehydration symptoms with DKA BS can't be converted to energy, large amounts of BS in BV draws water in and is p'd out leading to dehydration.
Why hypokalemia with DKA because of excess glucose draws water into BV and everything along with K gets p'd out
with DKA you are dryed out, flushed, hypokalemia Because you are dehydrated
late signs of DKA Kussmauls resp, lethargy, coma and hypotension
Why kussmauals with dka this is a later response if DKA is not treated and occurs d/t correcting acidosis and balancing pH by blowing off more co2.
Why hypotension with DKA cuz the excess Glucose draw all fluids into the blood stream and it was p'd out, leaving you dehydrated, less volume, decreased bp
Why lethargy/coma with DKA d/t acidosis
What are the three categories to treat DKA Fluids, insulin and electrolytes
Which fluids do you give first when treating DKA 0.9% saline or 0.45% saline to dilute BS...this can be done rapidsly to reverse dehydration
At what point do you change the type of IV fluid and why? once BS reach >250, you want to slow down the recovery by giving D5W IV
Reduces BS & prevents vascular collapse IV fluid replacements
when do you start insulin? give fluids first to corret dehydration, then start insulin
which insulin do you give regular IV drip
How much regular IV drip to you give? 5 to 10 units
titrate (measure or balance) reg iv drip according to what? with hourly BS results
How quickly can you lower BS? no more than 75mg/dl per hour
So if you can't exceed more than 75mg/dl per hour to lower BS, what if you start out at 700 then in an hour, it should not exceed 625; or 625 should be remaining.
which electrolytes are affected by DKA potassium, phosphorus, magnesium and calcium
what happens to potassium during DKA glucose gets excreted through urine and pulls potassium with it.
Treatement with insulin drives what? it drives K back into the cell
where do they get K from? Supplements are given that include K.
When giving K supplements, what do you need to do? Monitor closely
what hapens to phosphate and magnesium they plummet after therapy begins
If phosphate and magnesium plummet what happens? calcium decreases
Phosphate, Mg and Ca need what the levels need to be monitored and pt needs to be treated if they are low.
monitor DKA pt for what hourly glucose and ketones, ABG's to check pH, electrolytes q 4 hours, EKG (d/t potassium fluctuation), VS, I&O (d/t diuresis), neuros and cardiac assess
What is HHNK? hyperosmolar hyperglycemia
HHNK is seen with Type I or II? Type II
Is HHNK sudden or gradual gradual insideous onset- no symptoms until BS is dangerously high
Typical person with HHNK is type II and has all or some of the following conditions older, obese and/or renal impairment
What are triggers to HHNK? Infection MI, stroke, surgery, meds or stress
What are the symptoms of HHNK? No symptoms until BS reach 600 or higher
HHNK symptoms Dehydration (thirst, tachycardia, dry skin, hypotension, decreased skin turgo, altered mental status,etc), rapid shallow res, blurred vision, wt loss, p'ing lots
which has more sever hyperglycemia? DKA or HHNK? HHNK
which has acidosis, ketones and fruity breath? DKA or HHNK? DKA
With HHNK dehydration is more severe than DKA in that dehydration is more pronounced, and Neuro symptoms are worse
with DKA, acidosis is prevalent and has signs including ab pain, acetone/fruity breath, kussmauls resp, and ketones in urine.
Why does HHNK have more severe hyperglycemia than DKA r/t the fact the BS increases over a long period of time, gradual changes aren't noticeable at first.
Why does HHNk Have more severe neuro symptoms than DKA because BS levels are higher with HHNK in the brain and leads to high dehydration in the brain (remember, water follows glucose)
what is the diff between Kussmal resp (DKA) and shallow, rapids respiration (HHNK) Not deep like we see in DKA which is trying to balance the pH (r/t ketones)
Treatment for HHNK? same as DKA (Fluids first, insulin second and replace/monitor lytes)
HHNK d/t severe dehydration which condition would you give fluids more rapidly 1-3 liters over two hours? DKA or HHNK
Which condition would you give fluids of 250 to 1000 cc/hour? DKA or HHNK DKA- dehydration is sever, but not as bad as with HHNK
what would you monitor for HHNK? Cardiac and nueros, i&O's, vs, lytes q 4 hours, bs q 1 hr, abg's & ekg
which is an emergent situation? Hyper or hypoglycemia Hypo. Hyperglcemia is not emergent, but will cause complications if HIGH BS is prolonged
Hyperglycemia will have similar symptoms to hypo except you'll see difficult concentrating, Increased infections, poor wound healing.
Hyperglycemia and hypoglycemia similar sympoms Hunger...but not sudden hunger as you see with hypo, thirst, fatigue, polyuria
differences between hyper and hypo with hypo you have diaphoresis, and with hyper you will have vision changes.
Chronic complications of diabetes r/t macrovascular these are large vessels that include cardio, peripheral and cerebral
Cardio (macrovascular) complications as a result of dm 4x likely to get cardiac disease, atherosclerosis at a younger age, greater rate of restonsis following angioplasty, CVA is leading cause of death, silent mi (d/t neuropathy)
Cardio disease and diabetics this occurs when large vessels get a blockage causing HA, MI, angina- diabbetics have 2-4x greater chance of getting this d/t lipid build up
what does lipid build up have to do with diabetes diabetics build up lipids at a younger age and is more severe as this increases the chances of cardio disease
What is the relationship between pvd and dm? Peripheral vascular disease is more prevelant with someone who has dm becauase BV become atheroslcerotic, causing occlusions in arteries (especially in legs) and can lead to gangrene and amputation
what is pvd BV's atherosclerotic leading to occlusions of arteries. People with DM are at greater risk for developing this.
Why Cerebrovascular and diabetes? These are large vessels, and when circulation decreased in the brain, could lead to stroke.
Diabetes and Microvascular complications effects eyes
Diabetes affects which part of eye? retin...causes retinapathy
retinopathy major cause of legal blindness.
Small microvessels get damaged when they get blocked from blood flow, they degenerate and hemorrhage leading to what? retinal detachment (retinopathy)
Diabetes is 25x more likely to develop an eye problem...one of which causes a permanent blurry are in center of vision macular degeneration
Diabetics are likely to develop clouded vision called cataracts
microvascular complications that affects nerves neuropathy
Peripheral neuropathy Affects distal nerves first: Toes & feet
s/sx of peripheral neuropathy numbness, tingling, burning, pain and poor wound healing.
autonomic neuropathy Involves the CNS and affects organs such as heart, lungs, GI and kidneys.
Orthostatic hypotension - BP drops with position changes Autonomic nervous system affect of cardio function
Incompletely emptying the bladder d/t damaged nerve and not being able to feel the urge to expel remaining urine Autonomic nervous system causes neurogenic bladder
what is a side effect to neurogenic bladder? UTI
How is the ans affect the GI Nerves to the stomach are damaged can cause incomplete emptying of the stomach.
The ans affects the nerve to the stomach and causes vomiting, because the stomach no longer knows how to process food properly.
Nerve damage to large intestine = decrease peristalsis which results in constipation.
Nerve damage to the small intestine = causes diarrhea because food passes thru not digested properly.
Gastroparesis nerve damage to the stomach that slows down function of stomach and gives pt a full feeling after a small meal.
nephropathy Microvascular (capillary) damage in kidneys
Nephropathy occurs in 40% of type 1 and 10% of type II occurs within 15-20 years of onset if it is going to occur.
If nephropathy is going to occur, then when will it happen? 15 to 20 years after onset occurs
what is the earliest symptom of nephropathy Microalbuminuria- albumin is present in urine - large molecules that get past the filter d/t kidney impairment.
End stage renal disease albumin that continually filters into the urine will result.
People with DM have increased complication of Infections d/t increased BS makes them more susceptible to infection.
Why do people with DM have difficulty treating infections? related to poor circulation.
DM are susceptible to this condition that is found in skin folds, groin, axilla, etc yeast infections
Other considerations r/t dm sexual dysfunction
sexual dysfunction that causes back flow to bladder retrograde ejaculation
ED Erectile dysfunction d/t neuropathy (impotent)
lab assessment are Blood glucose test, urine test
What is a normal fBS <100
what fbs prediabetes 100-126
You have full blown dm if your FB reads > 126
2 hour post prandial 2 hours after meal test
2 hour post prandial is normal <140
2 hour post prandial is prediabetes > 140 but < 200
2 hour post prandial is full blown dm > 200
oral glucose tolerance test In AM, after 10 hour fast. It is an all day test that includes starting with fasting glucose level draw, then drink 75g of sugary water, then draw blood at intervals
Capillary blood glucose monitoring recommended for all diabetics using finger stick, cost is 50 cents, at least 4x/day
Glycosylated Hgb A1c is now called A1c 120 day glucose history- it looks at RBC lifespan is 120 days- glucose attaches to hgb.
urine tests include ketones, albumin and glucose
Ketones and albumin should not be in urine
Glucose a good screening tool, but pt's have different glucose thresholds, usual is 180.
A1c if it is higher than 6.5 to 7.0 % then this is an indication that a person has dm.
Before meals, BS should be 80-120 (ADA) or 70-110 (AACE)
1 - 2 hours post meal <180 bs (ADA) & <140 AACE
Bedtime BS 100- 140
BP s/b 130/85 (ADA) & 120/80 (AACE)
type 1 and exercise can increase BS d/t glycogenesis
Type II and exercise can decrease BS by increasing cho metabolism and reversing insulin resistance an exercising muscle will accept glucose into its cell for readily
how to plan exercise reg, moderate and 3-5 x/week
If BS is > 200 do you exercise? No
For type 1 dm:if ketones are detected in urine then do you exercise? No, because liver will release glycogen that converts to glucose, increasing bs (gluconeogenesis)
Novolog, humulog and apidra rapid acting insulin
Novolog onset 15 - 30
Humolog onset 10-20
apidra Onset 10-15
Which rapid acting insulin has peak of 1-3 hours? novolog
Which rapid acting insulin has peak of 0.5 - 2.5 hrs? Humalog
Which rapid acting insulin has peak of 1 -1.5 hrs? apidra
what is the average duration of humalog, novolog and apidra? 3-5 hours
Short acting insulins Regular
Novolin R & Humalin R Regular short acting insulins
what is the onset of novolin R and humulin R? 30 to 60 min
What is the peak of novolin R and humulin R? 1-5 hours
What is the duration of novolin R and humulin R? 6 - 10 hours
Short acting Regular insulin comes in how many units? U/100 = 100 units/ml U/500 = 500 units/ml
Intermediate acting insulin NPH Novolin N & Humulin N
Novolin N & humulin N onset is 1 to 2 hours
Novolin N & humulin N peak is 6 to 14 hours
Novolin N & humulin N duration is 16 to 24 hours
Basal intermediate Levemir
Basal long acting lantus
Levemir onset 3 to 4 hours
levemir peak 6 to 8 hours
Levemir duration 12 to 24 hours
Lantus onset 70 min
Lantus peak Peakless
lantus duration Up to 24 hours
Can basal insulins be mixed with otherinsulins? No
Can basal insulins be given iv or subq or both? Subq only
Humulin 70/30 70 nph 30 reg
Humulin 70/30 onset, peak, and duration reg Onset 10 min, Nph onset 1 to 2 hours, reg peak 1-3 hours Nph peak 6-14 reg duration 3-5 nph duration 16-24
rapd insulin onset 10-20 min average
rapid insulin peak 1-3 hours
rapid duration 3-5 hours
reg onset 30-60 min
reg peak 1-5 hrs
reg duration 6-10 hrs
NPH onset 1 to 2 hours
NPH peak 6 to 14 hours
NPH duration 16-24
Humulin or novolin 50/50 50 nph 50 reg
Humalog 75/25 75 Humulin N (Lispro suspension) 25 Humalog (lispro)rapid
humalog 50/50 50 Humulin N (Lispro suspension) 50 Humalog (lispro)rapid
Humulin N = Lispro suspension
Lispro Humulog rapid acting insulin
humulin or novolin 70/30 70%nph 30% reg
Novalog 70/30 70 is aspart suspenion 30 is aspart rapid
NPH can be mixed with regular (humulin/novlin) & rapid (lispro/aspart)
what is the first thing to do when mixing insulins? 1st roll or rotate NPH
Cloudy-clear-clear-cloudy is the correct sequence when mixing insulins? yes
What is the next thing you do when mixing insulins? Inject air into cloudy, then inject air into clear, draw from clear, then draw from cloudy
lispor humalog onset is 15 - 30 minutes
aspart (novolog) onset is 10-20 minutes
Glulisine (Apidra)onset 10 - 15 minutes
Lispro (humalog) peak 0.5 to 2.5 hours
Aspart (novolog)peak 1 to 3 hours
Glulisine (apidra) peak 1 to 3 hours
lispro (humalog) duration 3 to 6.5 hours
Aspart (novolog) duration 3 to 5 hours
Glulisine (apidra)duration 3 to 5 hours
What is the onset for Humulin R & Novolin R? 30 to 60 min
What is the peak for Humulin R & Novolin R? 1 to 5 hours
what is the duration for humulin R and Novolin R? 6 to 10 hours
Novolin N & Humulin N onset is? 1 to 2 hours
Novolin N & Humulin N peak is? 6 to 14 hours
Novolin & Humilin N duration is? 16 to 24 hours
Intermediate BASAL insulin Levemir (detemir) onset 3 to 4 hours
Intermediate BASAL insulin Levemir (detemir) peak 6 to 8 hours
Intermediate BASAL insulin Levemir (detemir) duration 12 to 24 hours
Long acting (basal) lantus (glargine) onset 70 minutes
Long acting (basal) lantus (glargine) peak peakless
Long acting (basal) lantus (glargine)duration up to 24 hours
what is a single daily injection? it is rare because it is not ideal; basically it is intermediate mixed with regular.
What is a two dose protocol of insulin regimens? It is a mix of intermediate with rapid or reg acting insulin
when do you give two dose protocol insulin? 2/3 before breakfast and 1/3 before supper
which is most coventional and most common? 2 dose protocol
Four dose insulin regime is? Regular insulin 30 minutes before the email or rapid acting at start of meal.
with four dose regimen, what do they base the number of units on? It is based on BS and anticipated CHO intake
which insulin regimen best mimics the pancrease the four dose regimen
In order to be successful in doing the 4 dose treatment, what is need from the pt? Commitement & motivation to do this 4 x daily
combination of insulin and oral agent is? An insulin regiment that only Type II diabetics can follow.
how does combo of insulin and oral work? the oral works in the background, some stimulate the pancreas, block the liver, enhance the ability of insulin to get into the cell
what is basal bolus insulin It is the use of a long action insulin (i.e. levemir or lantus) in combination with rapid. Rapid is given based on corrective and nutritional dose
Lantus and levemir are a slow release insulin over 24 hours and acts as te pancreas.
With basal - bolus insulin, which one is give first and when? the basal (levemir or lantus) commonly in the am.
When do you give bolus? given at mealtime and is based on nutritional and corrective
What is nutritional bolus dose mean? It is a meal time dose of rapid acting insulin based on how many CHO will be eaten.
what is the ratio of insulin to carb? 1 unit per every "#" grams of CHO
What is the corrective bolus dose mean? This is based on the BS reading and given units according to sliding scale.
When are corrective and nutritional doses given? they are given together, one is based on CHO intake plus the BS reading.
what type of insulin is used for insulin drip? Regular insullin only that can be given as continuous IV.
the change rate on an insulin drip is based on what? the change rate based on BS, monitored q 1 hr
When giving insulin drip how often do you check bs? monitored q1 hr
Which insulin regimen is a standing order for hospital pts only? insulin drip
Why is an insulin drip recommended? for cardio surgery to help control BS that can elevate from stress hormones. Pts who have this therapy have less infection and heal faster.
First generation of sulfonylureas rarely used d/t side effects They stimulate release of insulin from the pancreas, and increase tissue response to insulin with prolonged use.
What stimulates pancreas to release insulin and increases tissue response to insulin with prolonged use? first generation sulfonylureas
Tolinase (tolazamide) this is a first generation sulfonylureas
Orinase (tolbutamide) first genertaion sulfonylureas
diabanese (chlopropamide) first gen of sulfonaylureas
Second generation sulfonylureas does what? It stimulates pancrease to release insulin, increases tissue response to insulin, is more potent and less side effects.
What are some examples of second gen sulfonylureas? Glyburide (Glynase, diabeta, micronase) Glipizide (glucotrol) Glimepiride (amaryl)
How does insulin secretagogues (meglitindies & Glinides) work? Stimulates pancrease to release insulin, rapid acting and short duration and needs to be taken 0 to 30 minutes before the meal.
Prandin (repaGLINIDE) & starlix (NateGLINIDE) are what? insulin secretagogues that are rapid acting with a short duration and needs to be taken 0 to 30 min before the meal.
Which oral insulin has the greatest risk of causing hypoglycemia? Prandin (repaGLINIDE) & starlix (NateGLINIDE) because they are rapid acting and have a short duration.
An oral hypoglycemic agents include 1st and 2nd sulfonylureas & insulin secretetagous
Talinase, diabenese, and orinase oral hypoglycemic agent that is 1st generatioin of sulfanyeuras
Glyburide (glynase, diabeta, micronase) & glucotrol (Glipizide), Amaryl (Glimepiride) 2nd generation of sulfanylureas oral hypoglycemic agent.
prandin and starlix (the drugs ending in glinide) are oral hypoglycemic agents classified as insulin secretagogues
Whate are insulin sensitizers Biguanides and glitazones (thiazolidinediones)
Biguanides (insulin sensitizers) decreases glucose production from liver, improves cell SENSITIVITY to insulin as secondary affect, lowers blood lipids and increases HDL.
Nursing considerations of biguanides Give with meal, causes diarrhea and DC for radiolocial procedures and 48 hours thereafter.
Glucaphage (metformin) biguanide that decreases production from liver, improves cell sensitivty to insulin, reduces bad lipids and increases HDL.
Glucaphage (metformin) considerations Need to give with meal, causes diarrhea and need to dc this for radiological procedures and 48 hours.
Glucovance (metformin + glyburide) Metformin decreases glucose production in liver, and improves cell sensitivity to insulin. while glyburide stimulates pancreas to release insulin and improves tissue response to insulin.
Glitazones (thiazolidinedoines) Insulin sensitizer that increases cell sensitivitiy and response to insulin
what causes wt gain and edema glitazones, which is an insulin sensitizer that increases sensitivity & response to insulin.
Actos (pioglitazone) & avandia (rosiglitazone) (-glitazone) Glitazones drugs that are insulin sensitizers, increases cell sensitivity and response to insulin.
Actos and avianda (-glitazone ending drugs)nursing considerations need to monitor liver function and ldl and TG levels.
which insulin sensitizer drugs cause wt gain and edema? actos and aviandia (generic name ending in -glitazone)
Carbohydrate inhibitors do what? inhibit enzyme activity that breaks down CHO in intestines-slows absorption of cho
Precose (acarbose) is a carb inhibitor that works in the GI tract to block the absorption of CHO
what are side effects of precose (acarbose)? bloating/flatulence and increase risks of hypoglycemia
what if you take precose (acarbose) and your BS are severly low and you are conscious? put carb containing food underneath tongue as it will abosorb into the system without going into the GI tract
When glucose is in Blood what happens to K? it moves out of BV and into the intracellular compartments
enzyme inhibitors Januvia (sitagliptin phosphate) increases incretin hormone levels and prolongs incretin activity, which helps to regulate glucose homeostasis throughout the day.
what does encretin do? it is a hormone that helps regulate glucose homeostasis
what is januvia it inhibits enzymes resulting in an increase of incretin hormones, prolongs their activity, helping to regulate glucose homeostasis all day long
what else does januvia do beside increasing incretin levels and prolong incretin activity to maintain glucose homeostasis all day? It increases and prolongs insulin release in response to a meal and reduces hepatic glucose production
there is no associated wt gain with this drug januvia
what other drugs can be used with januvia? metformin and thiazolidenediones
what is onglyza (saxaglipton)? it is in the same class as januvia (DP4- enzyme inhibitor), except it can be used by remal patients.
pramlitinide (symlin) synthetic amylin
what is amylin a hormone that regulates glucoseafter the first 3 hours of eating.
This injectable synthetic amylin drug can be used by Type 1 & type II but Pramlitinide (symlin) does not stimulate pancrease, it stimulates amylin which regulates glucose
This amylin synthetic drug is used as an adjunt, not a replacement for insulin pramlitinide (symlin)
when do you give pralitinide (symlin)? 30 minutes before the meal in either the thigh or ab.
Exetantide (byetta) is for type II dm because you have to have a functioning pancrease before use.
what is exetanide (byetta) made from? saliva from a gila monster (aka lizard spit)
How is byetts (exetanide) given? thigh or ab about hour before breakfast & supper
which drug promotes insulin secretion, decreases glucagon secretion and improves CHO metabolism exenatide (byetta)
how does byetta work? it does 3 things: promotes insulin secretion, decreases glucagon secretion, improves CHO metabolism
What are some other pluses if on byetta? wt loss and decreased appetite
Can byetta be used with other drugs or insulins? can be used with some other oral agents, but not approved for use with insulin, thiazolidinediones, prandin and precose
Victoza (liraglutide) this is a pen (GLP-1) GLP1 is a hormone that is in the small intestine, releases when we eat and signals insulin and slows down food in stomach
Created by: Wends1984