Blood Glucose Agents Flashcards

(88 cards)

1
Q

Glucose Regulation

A

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.

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2
Q

Glucose Regulation –INSULIN

A

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

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3
Q

Glucose Regulation –GLUCAGON

A

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

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3
Q

Glucose Regulation –ENDOCANNABINOID RECEPTORS

A

Deep the body in a state of energy gain to prepare for stressful situations

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3
Q

Glucose Regulation –ADIPOCYTES

A

Secrete adiponectin, which increases insulin sensitivity, decreases release of glucose from liver and protects blood vessels from inflammation.

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4
Q

Glucose Regulation –CORTICOSTEROIDS

A

Decrease insulin sensitivity, increase glucose release, and decrease protein building.

Stress hormone, cortisol

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5
Q

Glucose Regulation – GROWTH HORMONE

A

Decreased insulin sensitivity, increases Free Fatty Acids, increases protein building.

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6
Q

Metabolic Changes Occurring When Insufficient Insulin is Released

A

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–>

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7
Q

Diabetes Mellitus – CHARACTERISTICS

A

Complex disturbances in metabolism

Affects carbohydrate, protein and fat metabolism

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8
Q

Diabetes Mellitus – CLINICAL SIGNS

A

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

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9
Q

Disorders associated with Diabetes (vascular damage)

A

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.

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10
Q

Type 1 Insulin Dependent Diabetes Mellitus (IDDM)

A

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

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11
Q

Type 2 Non-Insulin Dependent Diabetes Mellitus (NIDDM)

A

Usually occurs in mature adults

Has a slow and progressive onset

Decreased insulin sensitivity in peripheral cells (insulin resistance)

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12
Q

Diabetes Due to other causes

A

Hyperglycemia secondary to other causes

Medication–> corticosteroids, cystic fibrosis, pancreatitis

Gestational Diabetes–> in pregnancy

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13
Q

Signs and Symptoms of Hyperglycemia

A

Glycosuria
Polyuria
Polyphagia
Polydipsia
Frequent infections
Poor wound healing
Fatigue
Lethargy
Irritation

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14
Q

Signs of Impending Dangerous Complications of Hyperglycemia (DKA)

A

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

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15
Q

Hypoglycemia

A

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

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16
Q

Signs of Hypoglycemia

A

Hangry
Irritability or moodiness
Confusion
Hunger
Inability to concentrate
Dizziness
Shakiness
Sweating
Tachycardia

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17
Q

Insulin–> ACTIONS

A

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

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18
Q

Insulin –> INDICATIONS

A

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

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19
Q

Insulin –> CONTRAINDICATIONS

A

There are NO contraindications except episodes of hypoglycemia

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20
Q

Insulin –> CAUTION

A

Pregnancy and lactation

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21
Q

Insulin –> ADVERSE EFFECTS

A

Hypoglycemia and ketoacidosis

Local site reactions

Decreased blood potassium levels

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22
Q

Insulin –> DRUG-DRUG INTERATIONS

A

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

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23
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
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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
25
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
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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
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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
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Glargine (Lantus, Toujeo) Onset, Peak and Duration
Onset --> 60-70 min (pt need to eat) Peak--> none Duration --> 24 hrs
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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
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Detemir (Levemir) Onset, Peak and Duration
Onset --> 1-2 hrs (pt needs to eat) Peak--> 3-6 hrs (Re-assessment of patient for hypoglycemia)
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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
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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
33
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
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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
35
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
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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
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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
38
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)
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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)
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Sulfonylureas --> CONTRAINDICATION
All are absolute - Allergy - Diabetic complications --> insulin better - Type 1 DM --> no effect - Pregnancy and lactation--> need insulin
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Sulfonylureas --> ADVERSE EFFECTS
Hypoglycemia GI distress Allergic skin reaction
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Sulfonylureas --> Drug-Drug INTERACTIONS
Beta blocker--> mask S&S of hyperglycemia Alcohol--> altered blood sugar levels Herbal remedies--> alter blood sugar levels
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Biguanides--> INDICATION
- Type 2 diabetes, first-line medication choice. -METFORMIN
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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
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Biguanides--> CONTRAINDICATION
All are absolute -Hypersensitivity/allergy -Metabolic Acidosis -Severe renal impairment
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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
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Biguanides--> ADVERSE EFFECTS
Black box warning: lactic acidosis--> severe renal impairment GI effects URI Taste disturbance Dizziness, headache
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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
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DPP-4 inhibitors (-gliptin) --> ACTION Sitagliptin
Slow inaction of incretin hormones - Increases insulin release -Decreases glucagon release
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DPP-4 inhibitors (-gliptin) --> INDICATION Sitagliptin
treat type 2 diabetes, in addition to diet and exercise
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DPP-4 inhibitors (-gliptin) --> CONTRAINDICATION Sitagliptin
all are absolute - Hypersensitivity/allergy - type 1 DM or DKA These patients need insulin
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DPP-4 inhibitors (-gliptin) --> CAUTIONS Sitagliptin
Renal impairment--> reduce dose
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DPP-4 inhibitors (-gliptin) --> ADVERSE DRUG EFFECTS Sitagliptin
Drug effects are rarely reported
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DPP-4 inhibitors (-gliptin) --> DRUG-DRUG INTERACTION Sitagliptin
Other medications that lower blood glucose
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Meglitinides (-glinide)
Repaglinide Nateglinide
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Meglitinides (-glinide) --> ACTION
Stimulates insulin release from the beta cells in the pancreas -Repaglinide -Nateglinide
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Meglitinides (-glinide) --> INDICATION
treatment for type 2 DM, in addition to diet and exercise
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Meglitinides (-glinide) --> CONTRAINDICATION
All are absolute - Hypersensitivity/allergy - Type 1 DM or DKA Need insulin instead
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Meglitinides (-glinide) --> CAUTION
Pregnancy and lactation no adequate studies causes blood sugar to drop in infant
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Meglitinides (-glinide) --> ADVERSE EFFECTS
URI Headache arthralgia Nausea, diarrhea, hypoglycemia
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Meglitinides (-glinide) --> DRUG-DRUG INTERACTIONS
NUMEROUS
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SGLT-2 Inhibitors (-gliflozin) Canagliflozin
ACTION - blocks co-transporter system so glucose is not reabsorbed but is lost in the urine
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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
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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
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SGLT-2 Inhibitors (-gliflozin)--> CAUTIONS Canagliflozin
Lactation
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SGLT-2 Inhibitors (-gliflozin)--> ADVERSE EFFECTS Canagliflozin
Dehydration, hypotension UTIs, genital fungal infections DKA Lower limb amputation
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SGLT-2 Inhibitors (-gliflozin)--> DRUG-DRUG INTERATION Canagliflozin
Numerous
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Thiazolidinediones (-glitazone) Pioglitazone
ACTION - decrease insulin resistance in peripheral cells and liver - increase responsiveness to insulin
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Thiazolidinediones (-glitazone) --> INDICATION Pioglitazone
Treatment in type 2 DM, in addition to diet and exercise
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Thiazolidinediones (-glitazone) --> CONTRAINDICATION Pioglitazone
Moderate to severe heart failure May exacerbate HF
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Thiazolidinediones (-glitazone) --> CAUTION Pioglitazone
Liver impairment--> risk of hepatic injury
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Thiazolidinediones (-glitazone) --> ADVERSE EFFECTS Pioglitazone
URI Headaches, muscle pain Increased total cholesterol Rapid weight gain and edema (fluid retention)
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Thiazolidinediones (-glitazone) --> DRUG-DRUG INTERACTION Pioglitazone
Neumerous
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GLP-1 Agonists (-glutide & -natide)
Semaglutide Exenatide
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GLP-1 Agonists (-glutide & -natide)--> ACTION
Increase insulin release Decrease glucagon release slow GI emptying Semaglutide Exenatide
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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
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GLP-1 Agonists (-glutide & -natide)--> CONTRAINDICATION
Absolute - Type 1 DM or DKA - Pregnancy and lactation need to use insulin instead
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GLP-1 Agonists (-glutide & -natide)--> ADVERSE EFFECTS
GI effects Pancreatitis
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GLP-1 Agonists (-glutide & -natide)--> DRUG-DRUG INTERACTION
other antidiabetic medication--> increase hypoglycemia Oral medication: effects my be slowed--> due to decreased GI emptying
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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***
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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
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Glucose Elevating Agents--> Indication GLUCAGON
Treat hypoglycemia (less than 70 mg/dL)
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Glucose Elevating Agents--> CONTRAINDICATION GLUCAGON
Known allergy (absolute) Pregnancy--> no studies, weigh risk and benefits
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Glucose Elevating Agents--> CAUTION GLUCAGON
Lactation--> can cause hyperglycemia baby Hepatic dysfunction, renal dysfunction, cardiac disease
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Glucose Elevating Agents--> ADVERSE EFFECTS GLUCAGON
GI upset Alternating in BP
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Glucose Elevating Agents--> DRUG-DRUG INTERACTION GLUCAGON
Anticoagulants--> increase bleeding