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Free Online NCLEX Review for the Complete Idiot. LVN/LPN. Diabetes #5. Names of medications, categories, types (short, int., long), onset, peak, duration.

diabetes, diabetes mellitus, patholophysiology, pharmacology
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Insulin - Lispro (Humalog)
Rapid acting insulin
Onset: 15-30 minutes
Peak: 1-2 hours
Duration: 3-4 hours
Insulin - Aspart (Novolog)
Rapid acting insulin
Onset: 15-30 minutes
Peak: 1-3 hours
Duration: 3-5 hours
Insulin - Glulisine (Apidra)
Rapid acting insulin
Onset: 15-30 minutes
Peak: 1-3 hours
Duration: 3-5 hours
*Can be used in insulin pump.
Insulin Regular - Humulin R - Novolin R
Short acting insulin
Onset: 30-60 minutes
Peak: 2-4 hours
Duration: 6-8 hours
*Regular insulin can be administered intravenously, thus it is used in emergencies.
*Can be used in insulin pump.
Insulin - Glargine (Lantus)
Insulin - Detemir (Levemir)
Long acting basal insulin
Onset: 1-2 hours
PeakLESS
Duration: 24 hours
*used overnight and between meals, 9am & 9pm
*Do not mix with other insulin.
Insulin NPH (Novolin-N - Humulin-N - ReliOn N)
Intermediate acting insulin
Onset: 1-3 hours
Peak: 6-12 hours
Duration: 18-26 hours
*NPH is the only intermediate insulin suitable for mixing with short acting insulin.
Cloudy solution-gently roll between palms before administration. Short acting before long acting. (clear before cloudy)
Insulin Novolog Mix 70/30 (Neutral Protamine aspart and aspart)
Mixed insulin
Onset: 15-30 minutes
Peak: 2-10 hours
Duration: 12-16 hours
*70% NPH, 30% Regular
Sulfonylureas- Oral hypoglycemic agents;
1st Generation:
Tolbutamide (Orinase)
Tolazamide (Tolinase)
Chlorpropamide (Diabinese)
2nd Generation:
Glipizide (Glucotrol)
Glyburide (Diabeta, Micronase, Glynase)
Gimepiride (Amaryl)
Lower blood glucose by:
1. stimulating secretion of insulin from the pancreas
2. increasing the body's sensitivity or response to insulin
3. reducing the release of glucose from the liver
-Classified by generations based on potency, duration and drug interactions/SE
-Adverse effects: hypoglycemia (most likely with kidney or liver dysfxn), effects potentiated by ETOH, NSAIDs, Tagamet
*Safe with Metformin.
*Not used for gestational diabetes.
*Primary site of action: Pancreas
Meglitinides;
Repaglinide (Prandin)
Nateglinide (Starlix)
same MOA as sulfonylureas
*Requires functioning pancreatic beta cells.
Biguanides;
Metformin (Glucophage, Glucophage XR, Fotamet, Riomet)
MOA- lowers blood glucose by decreasing production of glucose in the liver:
--Enhances glucose uptake and utilization by muscle
--DOES NOT promote insulin release from the pancreas or cause hypoglycemia
-Onset several days; peak 2-4 weeks
-Adverse effects: abdominal bloating, nausea, vomiting, diarrhea, risk for lactic acidosis in pts with elevated creatinine
-NIC - monitor serum glucose levels; give 30 minutes AC
Other uses: prevent Type 2 DM, polycystic ovarian syndrome.
*Primary site of action: Liver.
Alpha-Glucosidase Inhibitors;
Acarbose (Precose)
Miglitol (Glyset)
MOA- Metabolized by intestinal bacteria and digestive enzymes; delay carbohydrate absorption from the small intestine.
*Primary site of action: Gut
Thiazolidinediones aka glitazones;
Rosiglitazone (Avandia)
Pioglitazone (Actos)
MOA: Increase insulin sensitivity at insulin receptor sites on the cell. Most appropriate for adults whose bodies produce insulin but cannot use it because of inadequate or ineffective receptor sites.
-onset & peak unknown, duration 12-24 hr
-Adverse Effects:
--*Risk of MI and heart-related deaths in people taking Avandia
--edema, wt gain, fluid retention, avoid if pt has liver dysfunction, elevated liver enzymes, raises plasma lipids (TG, LDL, HDL)
*Primary site of action: Muscle
What is the best treatment for Type 1 diabetes?
-Prevent longterm complications by keeping blood glucose and lipids under tight control.
1. Diet:
-CHO and Mono-fats together = 60-70% cal
-Protein= 10%
-Saturated fat < 10%
-Cholesterol < 300 mcg/day
-Total caloric intake spread evenly with meals spaced 4-5 hours apart
2. Regular exercise that includes monitoring blood glucose pre- and post-
3. Insulin replacement
What is the best treatment for Type 2 diabetes?
-Prevent longterm complications by keeping blood glucose and lipids under tight control.
-Diet & exercise (promotes glucose uptake by muscles)
-Weight loss
-drug therapy, if diet & exercise fail
--oral hypoglycemic agents
--insulin
--injectable hypoglycemic agents (ie. Byetta)
Incretin memetic exenatide injection
Ex. Exenatide (Byetta)
-MOA: enhances glucose dependent insulin secretion
-Indication: as adjunct to metformin or sulfonylurea or a combination therapy when have not achieved adequate glycemic control
-Stimulates glucose-dependent release of insulin, inhibits postprandial release of glucagon, and suppresses appetite
-Major SE are nausea and hypoglycemia
-Given SC within 1H of AM & PM meal(BID)
-Peak 2 hours, half life 2.4 hours
-Excreted unchanged in urine (contraindicated in ESRD)
-NOT GIVEN with Type 1 DM or DKA
Pramlintide (Symlin)
New injectable drug for DM
MOA: amylin (peptide hormone in the pancreas, released with insulin) mimetic, delays gastric emptying & suppresses glucagon secretion, decrease postprandial levels of glucose; lowers calorie intake by increasing satiety
Therapeutic use: supplement mealtime insulin (SC injection)
Adverse effects: hypoglycemia, nausea, injection site reaction
Gliptins
Ex.: Sitagliptin (Januvia)
MOA:
-increases insulin release by enhancing the activity of incretins
-Reduces glucagon release
-Decreases hepatic glucose production
onset: rapid, peak: 1-4 hr, duration: 24 hr
What are four major effects of insulin deficit?
1. Impaired carbohydrate metabolism-glucose can't enter the cell, serum becomes hyperglycemic
2. Impaired fat metabolism - fat broken down in cholesterol & phospholipids (ie. atherosclerosis) or ketone bodies (potential ketosis)
3. Impaired protein metabolism - can't store or synthesize protein, but increased catabolism causes muscle wasting, elevated BUN, aminoacidemia and multiple organ dysfunction
4. Fluid & electrolyte imbalance-increased serum glucose, inc. plasma osmotic P, fluid shift to intravascular compartment, intracellular dehydration (polydipsia)
Glucagon
Given to increase blood glucose (opposite of insulin)
-naturally produced by alpha cells of the pancreas
-break down of glycogen to glucose
decreases conversion of glucose to glycogen
-stimulates biosynthesis of glucose
-Administered parentally
-Used only if IV glucose is not an option
What are s/s of DKA?
Type 1 DM
-Rapid onset- 1 to 24 hours
-Polyuria, polydipsia, polyphagia
-Dehydration
--warm, dry skin
--tachycardia, weak, thready pulse
--acute weight loss
--hypotension
-Ketoacidosis
--Nausea and vomiting, anorexia
--Ketone breath -- sweet, fruity odor
--Mental status changes
---lethargy, fatigue, stupor, coma
COMPENSATION: Respiratory, Kussmaul's respirations (rapid, deep respirations)
What are lab values associated with DKA?
1. Hyperglycemia (>300 mg/dL)
2. Low bicarb (<15 mEq/L)
3. Low pH (<7.3)
4. Ketonemia (positive ketones or acetones in blood)
5. Ketonuria (ketones or acetones in urine)
What is HHNS?
Type 2 DM
-Hyperglycemic Hyperosmolar Nonketotic Syndrome
-Characterized by:
--Serum osmolality of 310 mOsm/L
--Serum glucose of >600 mg/dL
--Absence of ketoacidosis/ketones
--Associated with Type 2 diabetes mellitus (most common)
Rate of onset: 24 hours to 2 weeks
Dehydration: Dry mucous membranes and thirst
Neurologic manifestations: decreased level of consciousness (sometimes coma); potential for seizures
What are s/s of hyperglycemia?
weak, tired, polyuria, polydipsia, polyphagia, blurry vision, itchy dry skin, fruity-smelling breath
What are s/s of hypoglycemia?
-Impaired cerebral function
-H/A, altered emotional behavior
-Difficulty problem solving, feelings of vagueness,
-Slurred speech, impaired motor function,
-Seizures, coma
-Nervous, shaky, dizzy, confused, hunger, cold & clammy skin, tachycardia, irritability
Hemoglobin A1C
A serum blood test which reflects glucose level over the preceding 2-3 months that is a better indicator of glycemic control over time than the FBS
6% reflects pretty good control
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