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NRS 155 Intro to Pharm > Blood Glucose Agents > Flashcards

Blood Glucose Agents Flashcards

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
Q

Regular Route (Humulin R, Novolin R)
Onset, Peak and Duration

A

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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24
Q

NPH route (Novalin N)
Onset, Peak and Duration

A

Onset –> 1-1.5 hrs (pt needs to eat)

Peak –> 4-12 hrs (Re-assessment of patient for hypoglycemia)

Duration –> 24 hrs

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25
Q

Inhaled insulin (Afrezza)
Onset, Peak and Duration

A

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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26
Q

Lispro (Humalog)
Onset, Peak and Duration

A

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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27
Q

Aspart (Novolog)
Onset, Peak and Duration

A

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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28
Q

Glargine (Lantus, Toujeo)
Onset, Peak and Duration

A

Onset –> 60-70 min (pt need to eat)

Peak–> none

Duration –> 24 hrs

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29
Q

Glulisine (Apidra)
Onset, Peak and Duration

A

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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30
Q

Detemir (Levemir)
Onset, Peak and Duration

A

Onset –> 1-2 hrs (pt needs to eat)

Peak–> 3-6 hrs (Re-assessment of patient for hypoglycemia)

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31
Q

Combination Insulins
Onset, Peak and Duration

A

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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32
Q

Insulin–> ASSESS

A

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

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33
Q

Insulin –> NURSING DIGNOSIS

A

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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34
Q

Insulin –> IMPLEMENTATION

A

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
Q

Insulin –> IMPLEMENTATION continued

A

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

36
Q

Insulin –> EVALUATION

A

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

37
Q

Sulfonylureas

A

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
Q

Sulfonylureas –> ACTION

A

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)

39
Q

Sulfonylureas –> INDICATION

A

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)

40
Q

Sulfonylureas –> CONTRAINDICATION

A

All are absolute
- Allergy
- Diabetic complications –> insulin better
- Type 1 DM –> no effect
- Pregnancy and lactation–> need insulin

41
Q

Sulfonylureas –> ADVERSE EFFECTS

A

Hypoglycemia
GI distress
Allergic skin reaction

42
Q

Sulfonylureas –> Drug-Drug INTERACTIONS

A

Beta blocker–> mask S&S of hyperglycemia
Alcohol–> altered blood sugar levels
Herbal remedies–> alter blood sugar levels

43
Q

Biguanides–> INDICATION

A
  • Type 2 diabetes, first-line medication choice.
    -METFORMIN
44
Q

Biguanides –> ACTION

A

Decreases production and increased uptake of glucose

Lowers both basal and postprandial glucose levels

Decreases hepatic glucose production

Improves insulin sensitivity of peripheral cells

45
Q

Biguanides–> CONTRAINDICATION

A

All are absolute
-Hypersensitivity/allergy
-Metabolic Acidosis
-Severe renal impairment

46
Q

Biguanides–> CAUTIONS

A

All increase risk of lactic acidosis
-Hepatic impairment
-Excessive alcoholic intake
-NPO status
-Radiologic contrast (wait 48 hours)
- Age 65 and older
- Hypoxic State

47
Q

Biguanides–> ADVERSE EFFECTS

A

Black box warning: lactic acidosis–> severe renal impairment

GI effects
URI
Taste disturbance
Dizziness, headache

48
Q

Biguanides–> DRUG-DRUG INTERACTIONS

A

Alchohol
Carbonic anhydrase–> increase risk of lactic acidosis
iodine containing contrast media –> can cause AKI, hold for 48 hours before contract radiology

49
Q

DPP-4 inhibitors (-gliptin) –> ACTION
Sitagliptin

A

Slow inaction of incretin hormones
- Increases insulin release
-Decreases glucagon release

50
Q

DPP-4 inhibitors (-gliptin) –> INDICATION
Sitagliptin

A

treat type 2 diabetes, in addition to diet and exercise

51
Q

DPP-4 inhibitors (-gliptin) –> CONTRAINDICATION
Sitagliptin

A

all are absolute
- Hypersensitivity/allergy
- type 1 DM or DKA
These patients need insulin

52
Q

DPP-4 inhibitors (-gliptin) –> CAUTIONS
Sitagliptin

A

Renal impairment–> reduce dose

53
Q

DPP-4 inhibitors (-gliptin) –> ADVERSE DRUG EFFECTS
Sitagliptin

A

Drug effects are rarely reported

54
Q

DPP-4 inhibitors (-gliptin) –> DRUG-DRUG INTERACTION
Sitagliptin

A

Other medications that lower blood glucose

55
Q

Meglitinides (-glinide)

A

Repaglinide
Nateglinide

56
Q

Meglitinides (-glinide) –> ACTION

A

Stimulates insulin release from the beta cells in the pancreas

-Repaglinide
-Nateglinide

57
Q

Meglitinides (-glinide) –> INDICATION

A

treatment for type 2 DM, in addition to diet and exercise

58
Q

Meglitinides (-glinide) –> CONTRAINDICATION

A

All are absolute
- Hypersensitivity/allergy
- Type 1 DM or DKA
Need insulin instead

59
Q

Meglitinides (-glinide) –> CAUTION

A

Pregnancy and lactation
no adequate studies
causes blood sugar to drop in infant

60
Q

Meglitinides (-glinide) –> ADVERSE EFFECTS

A

URI
Headache
arthralgia
Nausea, diarrhea, hypoglycemia

61
Q

Meglitinides (-glinide) –> DRUG-DRUG INTERACTIONS

A

NUMEROUS

62
Q

SGLT-2 Inhibitors (-gliflozin)
Canagliflozin

A

ACTION
- blocks co-transporter system so glucose is not reabsorbed but is lost in the urine

63
Q

SGLT-2 Inhibitors (-gliflozin)–> INDICATION
Canagliflozin

A

type 2 DM treatment in addition to diet and exercise

Research being done on use in Type 1 DM–> not FDA approved

64
Q

SGLT-2 Inhibitors (-gliflozin)–> CONTRAINDICATION
Canagliflozin

A

Absolute
- Type 1 DM or DKA
- Severe renal impairment

Pregnancy (2nd and 3rd trimester) –> may cause adverse renal effects

65
Q

SGLT-2 Inhibitors (-gliflozin)–> CAUTIONS
Canagliflozin

A

Lactation

66
Q

SGLT-2 Inhibitors (-gliflozin)–> ADVERSE EFFECTS
Canagliflozin

A

Dehydration, hypotension
UTIs, genital fungal infections
DKA
Lower limb amputation

67
Q

SGLT-2 Inhibitors (-gliflozin)–> DRUG-DRUG INTERATION
Canagliflozin

A

Numerous

68
Q

Thiazolidinediones (-glitazone)
Pioglitazone

A

ACTION
- decrease insulin resistance in peripheral cells and liver

  • increase responsiveness to insulin
69
Q

Thiazolidinediones (-glitazone) –> INDICATION
Pioglitazone

A

Treatment in type 2 DM, in addition to diet and exercise

70
Q

Thiazolidinediones (-glitazone) –> CONTRAINDICATION
Pioglitazone

A

Moderate to severe heart failure
May exacerbate HF

71
Q

Thiazolidinediones (-glitazone) –> CAUTION
Pioglitazone

A

Liver impairment–> risk of hepatic injury

72
Q

Thiazolidinediones (-glitazone) –> ADVERSE EFFECTS
Pioglitazone

A

URI
Headaches, muscle pain
Increased total cholesterol
Rapid weight gain and edema (fluid retention)

73
Q

Thiazolidinediones (-glitazone) –> DRUG-DRUG INTERACTION
Pioglitazone

A

Neumerous

74
Q

GLP-1 Agonists (-glutide & -natide)

A

Semaglutide

Exenatide

75
Q

GLP-1 Agonists (-glutide & -natide)–> ACTION

A

Increase insulin release
Decrease glucagon release
slow GI emptying

Semaglutide
Exenatide

76
Q

GLP-1 Agonists (-glutide & -natide)–> INDICATION

A

Treat Type 2 DM in addition to diet and exercise

Reduce risk of major CV events in Type 2 DM

Semaglutide
Exenatide

77
Q

GLP-1 Agonists (-glutide & -natide)–> CONTRAINDICATION

A

Absolute
- Type 1 DM or DKA
- Pregnancy and lactation
need to use insulin instead

78
Q

GLP-1 Agonists (-glutide & -natide)–> ADVERSE EFFECTS

A

GI effects
Pancreatitis

79
Q

GLP-1 Agonists (-glutide & -natide)–> DRUG-DRUG INTERACTION

A

other antidiabetic medication–> increase hypoglycemia

Oral medication: effects my be slowed–> due to decreased GI emptying

80
Q

Glucose Elevating Agents

A

GLUCAGON

raise the blood level of glucose when severe hypoglycemia occurs (less then 70 mg/dL)

have insulin on standby for emergency use*

81
Q

Glucose Elevating Agents–> ACTIONS
GLUCAGON

A

Increase the blood glucose levels by decreasing insulin release and accelerating the breakdown of glycogen in the liver to release glucose

82
Q

Glucose Elevating Agents–> Indication
GLUCAGON

A

Treat hypoglycemia (less than 70 mg/dL)

83
Q

Glucose Elevating Agents–> CONTRAINDICATION
GLUCAGON

A

Known allergy (absolute)
Pregnancy–> no studies, weigh risk and benefits

84
Q

Glucose Elevating Agents–> CAUTION
GLUCAGON

A

Lactation–> can cause hyperglycemia baby

Hepatic dysfunction, renal dysfunction, cardiac disease

85
Q

Glucose Elevating Agents–> ADVERSE EFFECTS
GLUCAGON

A

GI upset

Alternating in BP

86
Q

Glucose Elevating Agents–> DRUG-DRUG INTERACTION
GLUCAGON

A

Anticoagulants–> increase bleeding

NRS 155 Intro to Pharm (3 decks)

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