Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
grcc ad 155
diabetes
| 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
Popular Nursing sets