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