Week 11 - Chapter 57 - Drugs for Diabetes Mellitus Flashcards

1
Q

Casual Plasma Glucose Test

A

For this test, blood can be drawn at any time, without regard to meals. Fasting is not required. Of note, the test can be performed in the office, using a finger-stick blood sample and the same type of test device employed by patients at home. A plasma glucose level that is 200 mg/dL or higher suggests diabetes. However, to make a definitive diagnosis, the patient must also display classic signs of diabetes: polyuria, polydipsia, and rapid weight loss. Ketonuria may also be present, but only if blood glucose is extremely high.

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2
Q

Conventional insulin therapy

A

1 or 2 injections a day for Type 1 Diabetes

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3
Q

C-Peptide (Connecting Peptide)

A
  • -Is a peptide loop that runs from the A chain to the B chain. C-Peptide along with Proinsulin make up a precursor to Insulin.
  • -Measurement of plasma C-peptide levels offers a way to assess residual capacity for insulin synthesis. Since commercial insulin preparations lack C-peptide, and since endogenous C-peptide is only present as a by-product of insulin biosynthesis, the presence of C-peptide in the blood indicates the pancreas is still producing some insulin of its own.
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4
Q

Diabetes Mellitus: Overview

A

-Disorder of carbohydrate metabolism
>Deficiency of insulin
>Resistance to action of insulin
-Sustained hyperglycemia, polyuria, polydipsia, ketonuria, and weight loss

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5
Q

Type 1 diabetes (T1DM)

A

> Often type 1 diabetes develops during childhood or adolescence, symptom onset is relatively abrupt
Primary defect is destruction of pancreatic beta cells due to autoimmune process

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6
Q

Type 2 diabetes (T2DM)

A

> Most prevalent form of diabetes
Accounts for 90% to 95% of all cases of diabetes
Affects approximately 22 million Americans
Insulin resistance and impaired insulin secretion

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7
Q

Gestational diabetes

A

> Appears in the mother during pregnancy and subsides rapidly after delivery
Managed in much the same manner as any other diabetic pregnancy

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8
Q

Complications of Diabetes

-Short Term

A

> Hyperglycemia
Ketoacidosis
Hypoglycemia

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9
Q

Complications of Diabetes

-Long Term
Macrovascular vs Microvascular damage

A
-Macrovascular damage
  >Heart disease
  >Hypertension
  >Stroke
  >Hyperglycemia
  >Altered lipid metabolism
-Microvascular damage
  >Retinopathy
  >Nephropathy
  >Sensory and motor neuropathy
  >Gastroparesis
  >Amputation secondary to infection (Glucose, Immune,  Neuorpathy)
  >Erectile dysfunction
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10
Q

Ways to Diagnose Diabetes

A
1. Hemoglobin A1c
Tests based on glucose:
2. Fasting plasma glucose (FPG) test
3. Casual plasma glucose test
4. Oral glucose tolerance test (OGTT)
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11
Q

Prediabetes

A

> Impaired fasting plasma glucose between 100 mg/dL and 125 mg/dL
Impaired glucose tolerance test
Increased risk for developing type 2 diabetes
May reduce risk with diet changes and exercise and possibly with certain oral antidiabetic drugs

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12
Q

Overview of Diabetes Treatment

A

> Primary goal is to prevent long-term complications
Tight control of blood glucose level is important
Controlling blood pressure and blood lipids also is important

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13
Q

Treatment of Type 1 Diabetes

A

-Requires a comprehensive plan
-Physical activity
-Insulin replacement
-Management of hypertension
>An ACE inhibitor (for example, lisinopril) or an ARB (for example, losartan) can reduce the risk of diabetic nephropathy
-Dyslipidemia
>Statins (for example, atorvastatin)

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14
Q

Treatment of Type 2 Diabetes

A

> Similar to type 1, requires comprehensive plan
Patient should be screened and treated for: -Hypertension, nephropathy, retinopathy, neuropathy, dyslipidemias
Glycemic control with: Modified diet and physical activity
Drug therapY

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15
Q

Tight Glycemic Control

Important

A
TGC - levels within normal range around-the-clock
Target goals:
1. A1C =  <7.0%
2. Premeal plasma glucose = 70-130 mg/dL
3. Peak postmeal plasma glucos = <180 mg/dL
-Beneficial for Young, Type-1 patients
-Inappropriate for:
  >Long-standing type 2 diabetes
  >Advanced microvascular or macrovascular complications
  >Extensive comorbid conditions
  >History of severe hypoglycemia
  >Limited life expectancy
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16
Q

Monitoring Treatment of Diabetes

Klimeki said this won’t be on the test but will probably see on NCLEX

A

-Self-monitoring of blood glucose (SMBG)
>Common target values for blood glucose
-70-130 mg/dL before meals
-100-140 mg/dL at bedtime

-Hemoglobin A1c
>Also called glycosylated hemoglobin or glycated hemoglobin
>Provides an index of average glucose levels over the prior 2 to 3 months
>A1c goal of below 7% is good for most patients
>Goal below 8% may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, or advanced microvascular or macrovascular complications

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17
Q

Complication of Poor Glucose Control

Diabetic Ketoacidosis

A

> Severe manifestation of insulin deficiency
Symptoms evolve quickly within hours or days
Most common complication in pediatric patients and leading cause of death
Characteristics: Hyperglycemia, Ketoacids, Hemoconcentration, Acidosis & Coma.
Treatment: Insulin, Bicarbonate, Fluids/Electrolytes.

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18
Q

Fasting Plasma Glucose Test

A

To determine FPG levels, blood is drawn at least 8 hours after the last meal. In normoglycemic individuals, FPG levels are less than 100 mg/dL. If FPG glucose levels are 126 mg/dL or higher, diabetes is indicated.

19
Q

Glycemic Index

What’s is it, and why is it important?

A

The glycemic index is an indicator of how a particular carbohydrate will affect blood glucose levels. Specifically, eating foods that have a high glycemic index (eg, white bread, unprocessed white rice) will raise glucose levels more rapidly and to a higher peak than will eating foods that have a low glycemic index (eg, rolled oats, 100% whole-wheat bread, lentils and legumes, most fruits and nonstarchy vegetables). In theory, foods with a low glycemic index should permit better glycemic control because, when glucose levels rise slowly after eating, the body has more time to process the glucose load. Importantly, this advantage is lost if total intake of low-index foods is excessive. Put another way, we may be able to achieve better glycemic control by consuming high-glycemic-index foods in moderate amounts rather than by consuming low-index foods in enormous amounts. The ADA states that substituting low-glycemic-index foods for higher-glycemic-index foods may modestly improve glycemic control.

20
Q

Glycosylated Hemoglobin

A

Another name for Hemoglobin A1c

21
Q

Hyperosmolar Hyperglycemic State (HHS)

a.k.a. Hyperglycemic Hyperosmolar Nonketotic Syndrome, (HHNS)

A

> Large amount of glucose excreted in urine results in dehydration and loss of blood volume
Increases blood concentrations of electrolytes and nonelectrolytes (particularly glucose); also increases hematocrit, Blood “thickens” and becomes sluggish
Compared to Diabetic Ketoacidosis
–Little or no change in ketoacid levels
–Little or no change in blood pH
–No sweet or acetone-like smell to urine or breath
Occurs most frequently with type 2 diabetes with acute infection, acute illness, or some other stress
Treatment: Correct hyperglycemia and dehydration with IV insulin, fluids, and electrolytes

22
Q

Impaired fasting plasma glucose

A

It’s a state of being prediabetic

-Parameters: 100 mg/dL and 125 mg/dL

23
Q

Impaired Glucose Tolerance

A

It’s a state of being prediabetic determined by the Oral glucose tolerance test (OGTT)

-Parameters: 140 mg/dL to 199 mg/dL

24
Q

Impaired Insulin Secretion

A

Symptom of Type II Diabetes. When insulin secretion is no longer tightly coupled to plasma glucose content: release of insulin is delayed and peak output is subnormal. More importantly, the target tissues of insulin (liver, muscle, adipose tissue) exhibit insulin resistance: For a given blood insulin level, cells in these tissues are less able to take up and metabolize the glucose available to them.

25
Q

Insulin Resistance

3 causes….

A
  1. Reduced binding of insulin to its receptors
  2. Reduced receptor numbers, and
  3. Reduced receptor responsiveness.

Over time, hyperglycemia leads to diminished pancreatic beta cell function, and hence insulin production and secretion eventually decline as the beta cells work harder to overcome insulin resistance within the tissues.

26
Q

Pancreatic beta cells

A

–the cells responsible for insulin synthesis and release into the bloodstream. In Type 1 diabetes, these cells are destroyed via the autoimmune process.

27
Q

Insulin lispro [Humalog]

A

> Short-Duration, Rapid-Acting Insulin

  • Analog of human insulin
  • Rapid onset (10-20 minutes) (won’t be tested on duration)
  • Short duration (3-5 hours)
  • Administered immediately before eating, possibly after eating
28
Q

Regular insulin [Humulin R, Novolin R]

A
Short-Duration, Slower-Acting Insulin
>Unmodified human insulin
>Effects begin in 30 to 60 minutes
>Peak in 1 to 5 hours
>Duration up to 10 hours
Dose:
-U-100 (100 units/mL) 
-U-500 (500 units/mL)
-CAUTION W U-500 and Pre-marked Insulin Syringe (they are usually marked based on U-100 strength)
29
Q

NPH insulin [Humulin N, Novolin N]

A

Intermediate-Duration Insulin
>Drug is injected twice or three times daily to provide glycemic control between meals and during the night
>NPH insulin is the only one suitable for mixing with short-acting insulins
>Allergic reactions are possible
>NPH insulins are cloudy suspensions that must be agitated before administration (don’t shake, roll between hands, bubbles make measurement inaccurate!)
>NPH insulins are administered by subQ injection only
Appearance:
>NPH insulin is a cloudy suspension

30
Q

Mixing Insulins

A

> NPH with short-acting insulins

>Short-acting insulin drawn first

31
Q

Insulin Administration

A
>Subcutaneous injection
   -Syringe and needle
   -Pen injectors
   -Jet injectors
>Subcutaneous infusion
   -Portable insulin pumps
>Intravenous infusion
   -Usually emergency, in-patient
>Inhalation
   -Available, Afrezza, mealtime coverage
32
Q

Insulin Storage

A

> Unopened vials should be stored under refrigeration until needed
Insulin should not be frozen
Insulin can be used until the expiration date if kept in the refrigerator

33
Q

Insulin: Therapeutic Use

A

> Indications

  • Principal: Diabetes mellitus
  • Required by all patients with T1DM and by many patients with T2DM
  • IV insulin for diabetic ketoacidosis
  • Gestational diabetes
  • Hyperkalemia: Can promote uptake of potassium
34
Q

Insulin: Physiology

A

> Biosynthesis
Secretion
Metabolic actions:
-Anabolic. Glucose upake into cells, Synthesis of glycogen, amino acids, triglycerides
Metabolic consequences of insulin deficiency:
-Reduced glucose uptake, intracellular catabolism.
-Glycogenolysis, gluconeogenesis, proteolysis, lipolysis (produces ketones, acetate)

35
Q

Insulin glargine [Lantus]

A

Long-Duration Insulin
>Modified human insulin
>Prolonged duration of action (up to 24 hours)
>Once-daily subQ dosing to treat adults and children with type 1 diabetes and adults with type 2 diabetes

36
Q

Type of Oral Hypoglycemic:

Metformin [Glucophage] - Biguanides

A

> First choice for most Type-2 patients. Can prevent onset in some groups.
Inhibits glucose production in liver, sensitizes insulin receptors (fat,muscle)

> Adverse effects:

  • GI upset. Lactic acidosis, rare, can be fatal. Low risk of hypoglycemia.
  • Decreased B12, Folic Acid Levels
37
Q

Type of Oral Hypoglycemic: Indication and Adverse effects

Glyburide [DiaBeta] - Sulfonylureas

A

> K+ channel blocking stimulates insulin release from Beta cells (Not in Type-1!)

> Adverse effects:
-Hypoglycemia, teratogenic, excreted in milk

38
Q

Type of Oral Hypoglycemic: Indication and Adverse effects

Repaglinide [Prandin] - Meglitinides/Glinides

A

-K+ channel blocking stimulates insulin release from Beta cells (Not in Type-1!

> Adverse effects
-Hypoglycemia

39
Q

Type of Oral Hypoglycemic: Indication and Adverse effects

Pioglitazone [Actos] - Thiazolidinediones/Glitazones

A

> PPAR-gamma agonists
Enhance response to insulin in targets (liver/muscle/fat) (Not in Type-1!)
Increased glucose uptake, decreased glucose production

> Adverse effects

  • Heart failure 2ndary to renal fluid retention
  • Hypoglycemia when used w insulin
  • Ovulation
  • Bladder Cancer
  • Fractures
40
Q

Type of Oral Hypoglycemic: Indication and Adverse effects

Acarbose [Precose] - Alpha-glucosidase inhibitors

A

> Act in the intestine to delay absorption of carbohydrates by inhibiting formation of monosaccharides from disaccharides
Type-2 only

> Adverse effects
-Frequently causes flatulence, cramps, abdominal distention, borborygmus, and diarrhea,…rarely liver dysfunction

41
Q

Type of Oral Hypoglycemic: Indication and Adverse effects

Sitagliptin [Januvia] - DPP-4 Inhibitors/Gliptins

A

> Enhances effects, by preventing breakdown, of “incretins” (endogenous hormones that stimulates glucose triggering of insulin release and suppress glucagon release)
Type-2

> Adverse effects:
-Well tolerated. Rarely pancreatitis

42
Q

Non-Insulin Injectable Drugs: Indication and Adverse effects

Exenatide [Byetta]

A

> GLP-1 receptor agonists (also called incretin mimetics)
-Slow gastric emptying, stimulate glucose-dependent release of insulin, inhibit postprandial release of glucagon, and suppress appetite

-Adverse effects: Hypoglycemia and gastrointestinal effects, including pancreatitis
Drug interactions

43
Q

Insulin Appearance

May be on exam, for sure on the NCLEX

A

Except for NPH insulins, all insulins made in the United States are formulated as clear, colorless solutions
NPH insulin is a cloudy suspension
Patients should inspect their insulin before using it and should discard the vial if the insulin looks abnormal

44
Q

Glucagon for Treatment of

Severe Hypoglycemia

A

-Preferred treatment is IV glucose
>Immediately raises blood glucose level
-Glucagon can be used if IV glucose is not available
>Delayed elevation of blood glucose
>Cannot correct hypoglycemia resulting from starvation
—Promotes glycogen breakdown, and the malnourished have little glycogen left