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Adv Pharm > Chaper 48: Diabetes Mellitus > Flashcards

Chaper 48: Diabetes Mellitus Flashcards

1
Q

Diabetes Mellitus: Overview of the Disease and Its Treatment

A

Disorder of carbohydrate metabolism
Deficiency of insulin
Resistance to action of insulin

Sustained hyperglycemia, polyuria, polydipsia, ketonuria, and weight loss

Ketones and weight loss with type I

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2
Q

TIDM

A

As a rule, type 1 diabetes develops during childhood or adolescence, and symptom onset is relatively abrupt -typically follows viral infection

Can develop during adulthood

Accounts for 5% of all cases of diabetes mellitus

Primary defect is destruction of pancreatic beta cells due to autoimmune process

Trigger for this immune response is not entirely known, but genetic, environmental, and infectious factors likely play a role

Need insulin replacement for life

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3
Q

TIIDM

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

Insulin resistance

Strong family association

Will not have ketone urea –will produce a little insulin to prevent ketoacidosis.

May need oral meds and insulin sup

typically overweight or obese at time of dx

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4
Q

Complications of DM

A

Short-term
Hyperglycemia
Ketoacidosis -Type I
Hypoglycemia

Long-term Macrovascular damage
Heart disease
Hypertension
Stroke
Hyperglycemia
Altered lipid metabolism

Long-term Microvascular damage
Retinopathy
Nephropathy: Angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB)
Sensory and motor neuropathy
Gastroparesis
Amputation secondary to infection
Erectile dysfunction

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5
Q

DM and preg

A

Before insulin: Virtually all babies born to severely diabetic women died during infancy

Factors during pregnancy
Placenta produces hormones that antagonize the actions of insulin
Production of cortisol increases threefold
Glucose can pass freely from the maternal to the fetal circulation (fetal hyperinsulinemia)
See lg infants (over 8lb)

Proper glucose levels are needed in the pregnant patient and in the fetus to prevent teratogenic effects
Want 3 month prior to conception if possible
Screening early preg visits

Fetal death frequently occurs near term

Earlier delivery is desirable

Baby may be hypoglycemic on delivery

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6
Q

Gestational DM

A

Appears in the mother during pregnancy and subsides rapidly after delivery
Managed in much the same manner as any other diabetic pregnancy
Blood glucose should be monitored and controlled with diet and insulin
Diabetic state usually disappears almost immediately after delivery
If diabetic state persists beyond delivery, it is no longer considered gestational and should be rediagnosed and treated accordingly
If pt has GDM, at much higher risk of dm as they age, typically type 2

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7
Q

DM dx

A

Hemoglobin A1c
3m average BG
6.5 or higher dx

Tests based on glucose:

Fasting plasma glucose (FPG) test
Criteria for dx would be over 126
Fast of 8hr

Casual plasma glucose test
Random plasma glucose
> 200 + s/sx of DM

Oral glucose tolerance test (OGTT)
2 hr test post carb load
>200 mg per deciliter considered dx

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8
Q

Prediabetes

A

Impaired fasting plasma glucose between 100 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
Many people who meet criteria for “prediabetes” never develop diabetes, even if they do not take precautions against diabetes
If overweight pt, weight loss can take them out of this category
May give metformin, lifestyle changes for 3m to see if they can move out of this category
Many do not develop DM

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9
Q

Overview of DM tx

A

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

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10
Q

Type 1 DM tx

A

Requires a comprehensive plan
Integrated program of diet, self-monitoring of blood glucose, exercise, and insulin replacement

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11
Q

TIDM dietary measures

A

Evidence suggests no ideal percentage of calories that should be ingested from carbohydrate, fat, or protein

Macronutrient distribution for any given individual is based on the person’s current eating patterns, preferences, and goals

Glycemic index

Substituting low-glycemic-load foods for higher-glycemic-load foods may modestly improve glycemic control

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12
Q

Physical activity for TIDM

A

150 min of exercise a week

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13
Q

Insulin requirements for TIDM

A

Lifelong replacement

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14
Q

TIDM HTN mgmt

A

An ACE inhibitor (e.g., lisinopril) or an ARB (e.g., losartan) can reduce the risk of diabetic nephropathy

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15
Q

TIDM dyslipidemia

A

Statins ex. Atrovastain

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16
Q

Type 2 DM tx

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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17
Q

When tight glycemic control is inapppropriate

A

Long-standing type 2 diabetes
Advanced microvascular or macrovascular complications
Extensive comorbid conditions
History of severe hypoglycemia
Limited life expectancy

May allow older adults to have higher hgA1c bc we don’t want them to develop hypoglycaemia ( worry about dizziness -> falls, fx)

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18
Q

Monitoring DM tx

A

Self-monitoring of blood glucose (SMBG)
Common target values for blood glucose
70 to 130 mg/dL before meals
100 to 140 mg/dL at bedtime
Needs to be individualized to pt
May let kids/YA run a higher BG bc of physical activity. Do not want them to be hypoglycaemic

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19
Q

Monitoring DM tx: HgA1C

A

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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20
Q

Metabolic consequences of insulin deficiency

A

Catabolic mode
Increased glycogenolysis
Increased gluconeogenesis
Reduced glucose utilization

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21
Q

Insulin preps

A

“High alert” agents

Recombinant DNA technology
Human insulin: Identical to insulin produced by the human pancreas
Human insulin analogs: Modified forms of human insulin that have the same pharmacologic actions as human insulin but different time courses

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22
Q

Short duration: rapid acting insulin

A

Insulin lispro [Humalog]
Insulin aspart [NovoLog]
Insulin glulisine [Apidra]
Looking at onset of 15min

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23
Q

Short duration: slower acting insulin

A

Regular insulin [Humulin R, Novolin R]
Onset: 30 min

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24
Q

intermediate duration insulin

A

Neutral protamine Hagedorn (NPH) insulin
Onset: 1-3hr
Needs to be taken BID

25
Q

Long duration insulin

A

Insulin glargine (Lantus)
Insulin detemir (Levemir)
Taken once/twice a day at same time each day
No peak

26
Q

Insulin lispro (humalong)

A

Analog of human insulin
Rapid onset (10 to 20 min)
Short duration (3 to 5 hr)
Administered immediately before eating or even after eating

Rapid-acting analog of regular insulin
Onset: 15 to 30 minutes after subcutaneous (subQ) injection
Duration: 3 to 6 hours
Usual route is subQ via injection or use of an insulin pump
Acts faster than regular insulin but has a shorter duration of action
Should be injected 5 to 10 minutes before meals

27
Q

Insulin glulisine [Apidra]

A

Synthetic analog of natural human insulin
Rapid onset (10 to 15 min)
Short duration (3 to 5 hr)
Should be administered close to the time of eating

28
Q

Regular insulin [Humulin R, Novolin R]

A

Unmodified human insulin
Four approved routes: SubQ injection, subQ infusion, intramuscular (IM) injection (used rarely), and oral inhalation (approved but not currently used)
Effects begin in 30 to 60 minutes
Peak in 1 to 5 hours
Duration up to 10 hours
Clear solution

U-100 (100 units/mL)
U-500 (500 units/mL)
Not used very often

29
Q

​NPH insulin [Humulin N, Novolin N]

A

Drug is injected twice or three times daily to provide glycemic control between meals and during the night
Usually 2x/day
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
NPH insulins are administered by subQ injection only

NPH, neutrall protamine Hagedorn.
70/30 combo -70 NPH, 30 regular

30
Q

Insulin glargine [Lantus]

A

Modified human insulin
Prolonged duration of action (up to 24 hr)
Once-daily subQ dosing to treat adults and children with type 1 diabetes and adults with type 2 diabetes
Clear solution

31
Q

Insulin detemir [Levemir]

A

Human insulin analog
Slow onset and dose-dependent duration of action
Used to provide basal glycemic control
Clear, colorless solution
Dosing: Once or twice daily by subQ injection
Do not mix with other insulins
Must not be given IV

32
Q

Insulin Appearance

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

33
Q

Insulin [ ]

A

100 units/mL (U-100)
500 units/mL (U-500)

34
Q

Mixing insulin

A

NPH with short-acting insulins
Short-acting insulin drawn first

35
Q

Insulin admin

A

Subcutaneous injection
Syringe and needle
Pen injectors
Jet injectors

Subcutaneous infusion
Portable insulin pumps
Implantable insulin pumps

Intravenous infusion

Inhalation
Not used as much

36
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

After opening, insulin can be kept up to 1 month without significant loss of activity

Insulin should be kept out of direct sunlight and extreme heat

Mixtures of insulin in vials are stable for 1 month at room temperature and for 3 months under refrigeration

Mixtures in prefilled syringes should be stored in a refrigerator for at least 1 week; they should be stored vertically with the needle pointing up

Roll before admin

37
Q

Insulin therapeutic use

A

Principal: Diabetes mellitus

Required by all patients with T1DM and by many patients with T2DM

Most insulin sold is used by people with type 2 diabetes, largely because T2DM accounts for 90% to 95% of all cases of diabetes

IV insulin for diabetic ketoacidosis

Gestational diabetes

Hyperkalemia: Can promote uptake of potassium

Aids in the diagnosis of growth hormone (GH) deficiency

38
Q

Insulin dosing schedule

A

Three dosing schedules:

Twice daily premixed insulin regimen

Intensive basal/bolus strategy

Continuous subcutaneous insulin
Insulin pump

39
Q

Achieving Optimal Glucose Control

A

Careful attention to all elements of the treatment program (diet, exercise, insulin replacement therapy)
A defined glycemic target
Self-monitoring of blood glucose according to the patient’s individualized management plan
A high degree of patient motivation
Extensive patient education
The responsibility for managing diabetes rests with the patient

40
Q

Complications of insulin tx -hypoglycemia

A

Hypoglycemia

Blood glucose below 70 mg/dL
Rapid treatment mandatory

Conscious patients: Fast-acting oral sugar (e.g., glucose tablets, orange juice, sugar cubes, nondiet soda)

If swallowing reflex or gag reflex is suppressed:
Nothing should be given by mouth
IV glucose or parenteral glucagon is the preferred treatment

Chocolate slows absorption of glucose

41
Q

Other compl of insulin tx

A

Lipohypertrophy
Allergic reactions
Hypokalemia

42
Q

Insulin drug interactions

A

Hypoglycemic agents
Hyperglycemic agents
Beta-adrenergic blocking agents
Harder for pt to recognize hypoglycemia

43
Q

Oral hypoglycemics

A

Biguanides
Metformin [Glucophage]

Sulfonylureas

Thiazolidinediones (also known as glitazones)
Rosiglitazone [Avandia]
Pioglitazone [Actos]

Meglitinides (also known as glinides)
Repaglinide [Prandin]
Nateglinide [Starlix]

44
Q

Metformin [Glucophage]

A

Drug of choice for initial therapy in most patients with type 2 diabetes

Most common side effects: Gastrointestinal (GI) disturbances
Lactic acidosis, a potentially fatal complication, is rare

Uses:
Prevention of type 2 diabetes
Gestational diabetes
Polycystic ovary syndrome (PCOS)

If pt is not tolerating metformin after 2-3 weeks, can try metformin ER
Metformin ER may have large copay or not be covered at all

45
Q

Sulfonylureas

A

First oral antidiabetics available

Promote insulin release

Can be used only for type 2 diabetes

Major side effects: Hypoglycemia, weight gain

First generation
Not used much at all

Second generation
Glymepirides, glyphosis, glyberides

Cardiotoxicity

If pt is allergic to sulfa AB should not be taking this

46
Q

Meglitinides (glinides)

A

Repaglinide [Prandin]
Generally well tolerated
Adverse effect: Hypoglycemia, weight gain
Drug interactions: Gemfibrozil [Lopid]

Nateglinide [Starlix]
Pharmacology nearly identical to that of repaglinide

Promote insulin secretion by pancreas

47
Q

Thiazolidinediones (glitazones)

A

Reduce glucose levels primarily by decreasing insulin resistance
Only indication is type 2 diabetes, mainly as an add-on to metformin
Rosiglitazone [Avandia]: Restricted use
Pioglitazone [Actos]

48
Q

Pioglitazone [Actos]

A

Reduces insulin resistance and may also decrease glucose production

Indication: Adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes

Adverse effects: Generally well tolerated; most common reactions are upper respiratory tract infection, headache, sinusitis, and myalgia

49
Q

Alpha-glucosidase inhibitors

A

Act in the intestine to delay the absorption of carbohydrates

Indication: Type 2 diabetes

Acarbose [Precose]
Adverse effects: Frequently causes flatulence, cramps, abdominal distention, borborygmus, diarrhea, and liver dysfunction

Miglitol [Glyset]
Especially effective among Latinos and African Americans
Adverse effects: Flatulence, abdominal discomfort, and other GI effects
Has not been associated with liver dysfunction

50
Q

DPP-4 inhibitors (also called gliptins)

A

Promote glycemic control by enhancing the actions of incretin hormones

Stimulate glucose-dependent release of insulin

Suppress postprandial release of glucagon

Decrease hepatic glucose production

Sitagliptin [Januvia]

DPP-4 , dipeptidyl peptidase-4.

SE: pancreatitis, hypersensitivity rxn

Don’t prescribe to someone with hx of pancreatitis

Saxagliptin [Onglyza]
Most common adverse effects: Upper respiratory infection, urinary tract infection, and headache

Linagliptin [Tradjenta]
Alogliptin [Nesina]

51
Q

Sodium-glucose cotransporter 2 (SGLT-2) inhibitors

A

Block reabsorption of filtered glucose in the kidney, leading to

Indication: Type 2 diabetes mellitus

Dapagliflozin [Farxiga]

Canagliflozin [Invokana]
Side effects: Genital fungal infections in female patients, urinary tract infections, increased urination, weight loss

Fungal infections, Etc cause people to d/c drug

52
Q

Other drugs for DM tx

A

Colesevelam [Welchol]
Bromocriptine

53
Q

Noninsulin Injectable Drugs

A

Pramlintide -Amylin mimetic
incretin mimetics

54
Q

GLP-1 receptor agonists (also called incretin mimetics)

A

Slow gastric emptying, stimulate glucose-dependent release of insulin, inhibit postprandial release of glucagon, and suppress appetite

Exenatide [Byetta]
Adverse effects: Hypoglycemia and gastrointestinal effects, including pancreatitis

Liraglutide [Victoza]
May cause medullary thyroid carcinoma (MTC)

55
Q

Amylin mimetics

A

Pramlintide [Symlin]
Reduces postprandial levels of glucose by delaying gastric emptying and suppressing glucagon secretion
Adverse effects: Hypoglycemia and nausea, injection site reactions

56
Q

Acute Complications of Poor Glycemic Control

A

Diabetic ketoacidosis (DKA)
Type 1

Hyperosmolar hyperglycemic state (HHS)
Type 2

Cardinal features of both conditions: Hyperglycemic crisis and associated loss of fluid and electrolytes
Both conditions can be life-threatening

Differences
Hyperglycemia is more severe in HHS
Ketoacidosis characteristic of DKA, absent in HHS

Treatment of the two disorders is similar

57
Q

Diabetic Ketoacidosis

A

Severe manifestation of insulin deficiency

Symptoms evolve quickly within hours or days

Most common complication in pediatric patients and the leading cause of death

Characteristics
Hyperglycemia
Ketoacids
Hemoconcentration
Acidosis
Coma

Altered glucose metabolism
Hyperglycemia
Water loss
Hemoconcentration

Altered fat metabolism

Treatment
Insulin replacement
Bicarbonate for acidosis
Water and sodium replacement
Potassium replacement
Normalization of glucose levels
Production of ketoacids

58
Q

Hyperosmolar Hyperglycemic State (HHS)

A

Also called hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

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

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

Can evolve slowly
Metabolic changes begin a month or two before signs and symptoms become apparent

If left untreated, can lead to coma, seizures, and death

Management
Correct hyperglycemia and dehydration with IV insulin, fluids, and electrolytes

More common in older adults

59
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

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