grcc ad 155 Word Scramble
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Question | Answer |
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
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