Blood Glucose Agents Flashcards
Glucose Regulation
Regulated by the pancreas
–> Endocrine Gland (our focus)–>
Produces hormones in the islets of Langerhans
Exocrine Gland
Released sodium bicarbonate and pancreatic enzymes directly into the common bile duct to be released into the small intestine
Neutralizes the acid chyme from the stomach and aids in digestion.
Glucose Regulation –INSULIN
Hormone produced by BETA cells of the islets of Langerhans
Released into circulation when levels of glucose around these cells RISE
Stimulates glycogen synthesis (production), conversion of lipids into fat stored as adipose tissue, and synthesis (production)
of proteins from amino acids.
Released AFTER meals, causing blood glucose levels to FALL
Glucose Regulation –GLUCAGON
The other hormone released by the pancreas
Released from alpha cells into islets of Langerhans in response to LOW blood glucose
Causes immediate mobilization of glycogen stored in the liver and RAISES blood glucose levels
Resp. due to low glucose levels
Glucose Regulation –ENDOCANNABINOID RECEPTORS
Deep the body in a state of energy gain to prepare for stressful situations
Glucose Regulation –ADIPOCYTES
Secrete adiponectin, which increases insulin sensitivity, decreases release of glucose from liver and protects blood vessels from inflammation.
Glucose Regulation –CORTICOSTEROIDS
Decrease insulin sensitivity, increase glucose release, and decrease protein building.
Stress hormone, cortisol
Glucose Regulation – GROWTH HORMONE
Decreased insulin sensitivity, increases Free Fatty Acids, increases protein building.
Metabolic Changes Occurring When Insufficient Insulin is Released
Hyperglycemia: Increased blood sugar
Glycosuria: Sugar is spilled into the urine
Polyuria: Increased urination
Polyphagia: Increased Hunger –> cells are starving
Polydipsia: increased thirst
Lipolysis: Fat breakdown
Ketosis: Ketones cannot be removed effectively
Acidosis: Liver cannot remove all the waste products–> body becomes acidotic–>
Diabetes Mellitus – CHARACTERISTICS
Complex disturbances in metabolism
Affects carbohydrate, protein and fat metabolism
Diabetes Mellitus – CLINICAL SIGNS
Hyperglycemia–> fasting blood sugar level greater than 126 mg/dL
Glycosuria –> if left untreated it can result in vascular damage
Long-term DM results in vascular damage
Disorders associated with Diabetes (vascular damage)
Atherosclerosis: Heart attacks and strokes related to development of atherosclerotic plaques in the vessel lining
Retinopathy: with resultant loss of vision as tiny vessels in the eye are narrowed and closed
Neuropathies: With motor and sensory changes in the feet and legs and progressive changes in other nerves as the oxygen is cut off
Nephropathy: With renal dysfunction related to changes in the basement membrane of the glomerulus
Infections: Increases in frequency and severity due to decreased blood flow and altered neutrophil function–> due to neuropathies
Foot ulcers: Decreased wound healing due to vascular insufficiency–> unnoticed wounds and infections due to neuropathy decreasing perception of pain.
Type 1 Insulin Dependent Diabetes Mellitus (IDDM)
Cannot make insulin efficiently
Usually a rapid onset; seen in younger people
Autoimmune destruction of the beta cells of the pancreas
Patients need insulin replacement
Type 2 Non-Insulin Dependent Diabetes Mellitus (NIDDM)
Usually occurs in mature adults
Has a slow and progressive onset
Decreased insulin sensitivity in peripheral cells (insulin resistance)
Diabetes Due to other causes
Hyperglycemia secondary to other causes
Medication–> corticosteroids, cystic fibrosis, pancreatitis
Gestational Diabetes–> in pregnancy
Signs and Symptoms of Hyperglycemia
Glycosuria
Polyuria
Polyphagia
Polydipsia
Frequent infections
Poor wound healing
Fatigue
Lethargy
Irritation
Signs of Impending Dangerous Complications of Hyperglycemia (DKA)
Fruity breath as the ketones build up in the system and are excreted through the lungs
Dehydration as the fluid and important electrolytes are lost through the kidneys
Increased, depth and rate of breathing (Kussmaul’s respiration)–> Hyperventilation–> as the body tries to rid itself of high acid levels
Loss of orientation and come–> Even death
Hypoglycemia
Blood glucose below 70 mg/dL
Initial response is parasympathetic stimulation, followed by “fight or flight” reaction
Breakdown of fat and glycogen to release glucose
Pancreas releases glucagon to increase glucose and somatostatin
Signs of Hypoglycemia
Hangry
Irritability or moodiness
Confusion
Hunger
Inability to concentrate
Dizziness
Shakiness
Sweating
Tachycardia
Insulin–> ACTIONS
Hormone that promotes the storage of the body’s fuels
Facilities the transports of various metabolites and ions across cell membranes
Stimulates the synthesis of glycogen from glucose
Reacts with specific receptor sites on the cells
Insulin –> INDICATIONS
Treatment of type 1 DM–> need exogenous (outside) source of insulin
Treatment of type 2 DM in patients whose diabetes cannot be controlled by diet and other agents
Insulin –> CONTRAINDICATIONS
There are NO contraindications except episodes of hypoglycemia
Insulin –> CAUTION
Pregnancy and lactation
Insulin –> ADVERSE EFFECTS
Hypoglycemia and ketoacidosis
Local site reactions
Decreased blood potassium levels
Insulin –> DRUG-DRUG INTERATIONS
Any drug that decreases glucose levels
Beta blockers –> block sympathetic NS
Thiazide diuretic –> will increase blood glucose level–> patient will need increase dose of insulin
Glucocorticoids –> will increase blood glucose level–> patient will need increase dose of insulin
Regular Route (Humulin R, Novolin R)
Onset, Peak and Duration
Onset –> 30 to 60 min (pt needs to eat)
Peak –> 2-4 hours –> most likely to experience hypoglycemia. Re-assessment of patient
Duration –> 6-12 hours
NPH route (Novalin N)
Onset, Peak and Duration
Onset –> 1-1.5 hrs (pt needs to eat)
Peak –> 4-12 hrs (Re-assessment of patient for hypoglycemia)
Duration –> 24 hrs
Inhaled insulin (Afrezza)
Onset, Peak and Duration
Onset–> 12-15 min (pt needs to eat)
Peak–> 60 min (re-assessment of patient for hypoglycemia)
Duration 2.5- 3hrs
Lispro (Humalog)
Onset, Peak and Duration
Onset –> 15 min (pt needs to eat)
Peak–> 30-90 min (re-assessment of patient for hypoglycemia)
Duration 2-5 hours
Aspart (Novolog)
Onset, Peak and Duration
Onset–> 10-20 min (pt needs to eat)
Peak–> 1-3 hrs (re-assessment of patient for hypoglycemia)
Duration –> 3-5 hrs
Glargine (Lantus, Toujeo)
Onset, Peak and Duration
Onset –> 60-70 min (pt need to eat)
Peak–> none
Duration –> 24 hrs
Glulisine (Apidra)
Onset, Peak and Duration
Onset –> 2-5 min (pt needs to eat)
Peak –> 30-90 min (Re-assessment of patient for hypoglycemia)
Duration–> 2 hrs
Detemir (Levemir)
Onset, Peak and Duration
Onset –> 1-2 hrs (pt needs to eat)
Peak–> 3-6 hrs (Re-assessment of patient for hypoglycemia)
Combination Insulins
Onset, Peak and Duration
Varies in onset, Peak and duration
Humalog 50/50, Humalog 75/25, NovoLog 70/30, Humulin 70/30, Novolin 70/30
faster/longer
Insulin–> ASSESS
Can lower potassium levels
Contraindications or cautions
skin lesion; orientation and reflexes; baseline pulse and blood pressure respiratory status (inhaled)
Investigate nutritional intake
Assess activity level, inducing amount and degree of exercise
Obtain blood glucose levels as ordered; monitor Hgb A1C, urinalysis (looking for glucose/ketones), and BMP
before meals and at bedtime
Insulin –> NURSING DIGNOSIS
Glucose and electrolyte imbalance risk related to the use of insulin and underlying diseases processes
Malnutrition risk related to changes in glucose transport
Altered sensory perception (kinesthetic, visual, auditory, and tactile) related to glucose levels
Infection risk related to injections and disease processes
Injury risk related to potential hyperglycemia or hypoglycemia and injection technique
coping impairment related to diagnosis and the need for injection therapy
Knowledge deficit risk regarding drug therapy
Insulin –> IMPLEMENTATION
ensure the patient is following a dietary and exercise regimen and is using good hygiene practices
Gently rotate the vial containing the agent and avoid vigorous shaking
Select a site that is free of bruising and scarring
Give maintenance dosed by the subcutaneous or inhaled routes only; rotate injection sites regularly
Monitor response carefully (finger stick)
Monitor the patient for signs and symptoms of hypoglycemia, especially during peak insulin times
Always verify the name of the insulin being given
Insulin –> IMPLEMENTATION continued
Use caution when mixing types of insulin
Store insulin an a cool place away from direct sunlight
Monitor the patients food intake; ensure that the patient eats when using insulin
Monitor the patients exercise and activities
Protect the patient from infection, including good skin care and foot care
Monitor the patients sensory losses
Help the patient to deal with necessary lifestyle changes
Instruct patients who are also receiving beta blockers about ways to monitor glucose levels and signs and symptoms of glucose abnormalities
Provide through patient teaching (hypo and hyper glycemia
Insulin –> EVALUATION
Monitor patient response to the drug (stabilization and blood glucose levels)
Monitor for adverse effects (hypoglycemia, ketoacidosis, lung function decline with inhaled insulin, and injection site irritation
Evaluate the effectiveness of the teaching plan (patient can name drug, dosage, adverse effects to watch for, specific measures to avoid them, and proper administration technique
Monitor compliance with regimen (monitor glucose levels, hemoglobin A1C
Sulfonylureas
Tolbutamide –> not often used–> 1st generation
Associated with increased risk of CV disease
Glipizide–> safer than 1st generation
Glyburide–> safer than 1st generation
Do not interact with as many protein bound drugs
have a longer duration of action, making it possible to take them only once or twice a day
Sulfonylureas –> ACTION
Stimulate insulin release from the beta cells in the pancreas
They improve binding to insulin receptors
-Tolbutamide (1st generation)
-Glipizide (2nd generation, better)
-Glyburide (2nd generation, better)
Sulfonylureas –> INDICATION
Lower blood glucose levels in type 2 diabetes
Used in addition to diet and exercise
-Tolbutamide (1st generation)
-Glipizide (2nd generation, better)
-Glyburide (2nd generation, better)
Sulfonylureas –> CONTRAINDICATION
All are absolute
- Allergy
- Diabetic complications –> insulin better
- Type 1 DM –> no effect
- Pregnancy and lactation–> need insulin
Sulfonylureas –> ADVERSE EFFECTS
Hypoglycemia
GI distress
Allergic skin reaction
Sulfonylureas –> Drug-Drug INTERACTIONS
Beta blocker–> mask S&S of hyperglycemia
Alcohol–> altered blood sugar levels
Herbal remedies–> alter blood sugar levels
Biguanides–> INDICATION
- Type 2 diabetes, first-line medication choice.
-METFORMIN
Biguanides –> ACTION
Decreases production and increased uptake of glucose
Lowers both basal and postprandial glucose levels
Decreases hepatic glucose production
Improves insulin sensitivity of peripheral cells
Biguanides–> CONTRAINDICATION
All are absolute
-Hypersensitivity/allergy
-Metabolic Acidosis
-Severe renal impairment
Biguanides–> CAUTIONS
All increase risk of lactic acidosis
-Hepatic impairment
-Excessive alcoholic intake
-NPO status
-Radiologic contrast (wait 48 hours)
- Age 65 and older
- Hypoxic State
Biguanides–> ADVERSE EFFECTS
Black box warning: lactic acidosis–> severe renal impairment
GI effects
URI
Taste disturbance
Dizziness, headache
Biguanides–> DRUG-DRUG INTERACTIONS
Alchohol
Carbonic anhydrase–> increase risk of lactic acidosis
iodine containing contrast media –> can cause AKI, hold for 48 hours before contract radiology
DPP-4 inhibitors (-gliptin) –> ACTION
Sitagliptin
Slow inaction of incretin hormones
- Increases insulin release
-Decreases glucagon release
DPP-4 inhibitors (-gliptin) –> INDICATION
Sitagliptin
treat type 2 diabetes, in addition to diet and exercise
DPP-4 inhibitors (-gliptin) –> CONTRAINDICATION
Sitagliptin
all are absolute
- Hypersensitivity/allergy
- type 1 DM or DKA
These patients need insulin
DPP-4 inhibitors (-gliptin) –> CAUTIONS
Sitagliptin
Renal impairment–> reduce dose
DPP-4 inhibitors (-gliptin) –> ADVERSE DRUG EFFECTS
Sitagliptin
Drug effects are rarely reported
DPP-4 inhibitors (-gliptin) –> DRUG-DRUG INTERACTION
Sitagliptin
Other medications that lower blood glucose
Meglitinides (-glinide)
Repaglinide
Nateglinide
Meglitinides (-glinide) –> ACTION
Stimulates insulin release from the beta cells in the pancreas
-Repaglinide
-Nateglinide
Meglitinides (-glinide) –> INDICATION
treatment for type 2 DM, in addition to diet and exercise
Meglitinides (-glinide) –> CONTRAINDICATION
All are absolute
- Hypersensitivity/allergy
- Type 1 DM or DKA
Need insulin instead
Meglitinides (-glinide) –> CAUTION
Pregnancy and lactation
no adequate studies
causes blood sugar to drop in infant
Meglitinides (-glinide) –> ADVERSE EFFECTS
URI
Headache
arthralgia
Nausea, diarrhea, hypoglycemia
Meglitinides (-glinide) –> DRUG-DRUG INTERACTIONS
NUMEROUS
SGLT-2 Inhibitors (-gliflozin)
Canagliflozin
ACTION
- blocks co-transporter system so glucose is not reabsorbed but is lost in the urine
SGLT-2 Inhibitors (-gliflozin)–> INDICATION
Canagliflozin
type 2 DM treatment in addition to diet and exercise
Research being done on use in Type 1 DM–> not FDA approved
SGLT-2 Inhibitors (-gliflozin)–> CONTRAINDICATION
Canagliflozin
Absolute
- Type 1 DM or DKA
- Severe renal impairment
Pregnancy (2nd and 3rd trimester) –> may cause adverse renal effects
SGLT-2 Inhibitors (-gliflozin)–> CAUTIONS
Canagliflozin
Lactation
SGLT-2 Inhibitors (-gliflozin)–> ADVERSE EFFECTS
Canagliflozin
Dehydration, hypotension
UTIs, genital fungal infections
DKA
Lower limb amputation
SGLT-2 Inhibitors (-gliflozin)–> DRUG-DRUG INTERATION
Canagliflozin
Numerous
Thiazolidinediones (-glitazone)
Pioglitazone
ACTION
- decrease insulin resistance in peripheral cells and liver
- increase responsiveness to insulin
Thiazolidinediones (-glitazone) –> INDICATION
Pioglitazone
Treatment in type 2 DM, in addition to diet and exercise
Thiazolidinediones (-glitazone) –> CONTRAINDICATION
Pioglitazone
Moderate to severe heart failure
May exacerbate HF
Thiazolidinediones (-glitazone) –> CAUTION
Pioglitazone
Liver impairment–> risk of hepatic injury
Thiazolidinediones (-glitazone) –> ADVERSE EFFECTS
Pioglitazone
URI
Headaches, muscle pain
Increased total cholesterol
Rapid weight gain and edema (fluid retention)
Thiazolidinediones (-glitazone) –> DRUG-DRUG INTERACTION
Pioglitazone
Neumerous
GLP-1 Agonists (-glutide & -natide)
Semaglutide
Exenatide
GLP-1 Agonists (-glutide & -natide)–> ACTION
Increase insulin release
Decrease glucagon release
slow GI emptying
Semaglutide
Exenatide
GLP-1 Agonists (-glutide & -natide)–> INDICATION
Treat Type 2 DM in addition to diet and exercise
Reduce risk of major CV events in Type 2 DM
Semaglutide
Exenatide
GLP-1 Agonists (-glutide & -natide)–> CONTRAINDICATION
Absolute
- Type 1 DM or DKA
- Pregnancy and lactation
need to use insulin instead
GLP-1 Agonists (-glutide & -natide)–> ADVERSE EFFECTS
GI effects
Pancreatitis
GLP-1 Agonists (-glutide & -natide)–> DRUG-DRUG INTERACTION
other antidiabetic medication–> increase hypoglycemia
Oral medication: effects my be slowed–> due to decreased GI emptying
Glucose Elevating Agents
GLUCAGON
raise the blood level of glucose when severe hypoglycemia occurs (less then 70 mg/dL)
have insulin on standby for emergency use*
Glucose Elevating Agents–> ACTIONS
GLUCAGON
Increase the blood glucose levels by decreasing insulin release and accelerating the breakdown of glycogen in the liver to release glucose
Glucose Elevating Agents–> Indication
GLUCAGON
Treat hypoglycemia (less than 70 mg/dL)
Glucose Elevating Agents–> CONTRAINDICATION
GLUCAGON
Known allergy (absolute)
Pregnancy–> no studies, weigh risk and benefits
Glucose Elevating Agents–> CAUTION
GLUCAGON
Lactation–> can cause hyperglycemia baby
Hepatic dysfunction, renal dysfunction, cardiac disease
Glucose Elevating Agents–> ADVERSE EFFECTS
GLUCAGON
GI upset
Alternating in BP
Glucose Elevating Agents–> DRUG-DRUG INTERACTION
GLUCAGON
Anticoagulants–> increase bleeding
