Ch 47 Antidiabetics

Question 1

diabetes mellitus

Answer 1

-chronic (result of deficient glucose metabolism due to insufficient insulin secretion beta cells)

Question 2

how many dm dx

Answer 2

according to WHO: amount rose from 108 mil in 1980 to 422 mil in 2014.
in 2016, estimated 1.6mil deaths by DM
2.2 mil were attributed to high glucose in 2012
almost 1/2 of all deaths attributable to high blood glucose before 70 yrs. who estimates dm as 7th leading COD in 2016

Question 3

dm is leading cause of?

Answer 3

blindness
renal failure
heart attacks
strokes
lower extremity amputations

Question 4

how to prevent or delay onset of type 2 dm

Answer 4

healthy diet
regular phsyical activity
maintaining normal body weight
avoiding tobacco use

Question 5

how to treat/delay/avoid consequences of DM

Answer 5

diet: always eat whole fruit and with protein
physical activity
meds
regular screening/tx for complications

Question 6

dm characterizations

Answer 6

polyuria
polydipsia
polyphagia

Question 7

types of DM

Answer 7

type 1(former juvenile-onset)
type 2
secondary diabetes
gestational diabetes mellitus

Question 8

type 1

Answer 8

A. Autoimmune disorder: body develops antibodies against insulin and/or pancreatic beta cells producing insulin
B. Body does not produce insulin

Question 9

type 2

Answer 9

A. Most common type
B. Heredity and obesity are major risk factors
C. Gestational diabetes is precursor
D. Some beta-cell function with fluctuating amounts of insulin secretion
E. Controlled with oral anti-diabetics: some may need insulin
F. Long term complications to be screened for retinopathy and peripheral neuropathy. Risk for delayed wound healing and coronary heart disease.

Question 10

secondary diabetes

Answer 10

A. May be caused by medications such as:
a. Glucocorticoids (prednisone, cortisone), thiazide diuretics and epinephrine
B. Hormonal changes

Question 11

gestational diabetes mellitus (GDM)

Answer 11

A. Develops during pregnancy, 24 to 28 weeks gestation.
-glucose levels generally normal 6 weeks postpartum.
-Need to test annually to ensure not become Type 2 Diabetic for 5 to 10 years after birth of fetus (increased risk).
C. Detected with impaired glucose tolerance

Question 12

antidiabetic drugs

Answer 12

used to control diabetes

d. Two groups of antidiabetic agents
i. Insulin
ii. Oral hypoglycemic (antidiabetic) drugs

Question 13

insulin

Answer 13

i. Released from beta cells of islets of Langerhans: response to increase in
blood glucose (BG)
ii. Oral glucose: more effective in raising serum insulin than IV glucose
iii. Insulin promotes uptake of glucose, amino acids, and fatty acids > converts to substances stored in the body
iv. Glucose is converted to glycogen in the liver and muscle, then stored for future glucose needs. This process lowers the amount of glucose in the blood

Question 14

normal range of fasting BG

Answer 14

Normal range of fasting blood glucose is 70-99 mg/dL OR 70-110 mg/dL for serum glucose (this range may differ slightly depending on hospital policy)

Question 15

at what range may glycosuria occur

Answer 15

If glucose is >180 mg/dL glycosuria may occur

Question 16

american diabetes association recommendation for dx

Answer 16

A. Several ways to diagnose: usually need test repeated to confirm diagnosis
B. May also diagnose if patient has classic symptoms in addition to (1) positive test
tests: hba1c, fasting plasma glucose, oral glucose tolerance test

Question 17

hba1c values

Answer 17

normal <5.7%
pre-dibaetic >5.7-6.4%
diabetes 6.5 or ^

Question 18

hba1c reflects avg plasma glucose up to?

Answer 18

3 months

Question 19

fasting plasma glucose values

Answer 19

normal <100
pre diabetic >100-125
diabetes 126 or ^

Question 20

oral glucose tolerance test (OGTT) values

Answer 20

normal <140
pre diabetic >140-199
diabetic 200 or ^

Question 21

beta cell secretion of insulin values

Answer 21

Beta cells in pancreas  secrete 0.2-0.5 units/kg/day of insulin

Question 22

commercially prepared insulin

Answer 22

i. Manufactured biosynthetically using recombinant DNA technology
ii. Human insulin > duplicates insulin produced by pancreas of human body
iii. Examples of Human insulins include:
A. Humulin R > only one that can be administered IV for a push or infusion
B. Novolin N
iv. Insulin syringes are typically marked in units of 100 units per 1 mL or 50 units per 0.5 mL
v. Insulin comes in 10ml vials

Question 23

administering insulin

Answer 23

i. not PO: GI secretions destroy insulin structure
ii. subQ: Abdominal injections are absorbed faster, but may also be given in deltoid, thigh, buttock (Site and depth affect absorption)
only regular insulin can be given IV.
iv. 45-90-degree angle
vi. Insulin injection sites must be rotated to prevent lipodystrophy (Tissue atrophy (depression) or hypertrophy (raised lump)) Per ADA, recommendation to daily injection at a specific location for 1 week

Question 24

insulin during illness

Answer 24

Increased need for insulin during periods of stress and illness
B. Should never withhold insulin without checking with provider during illness: hyperglycemia and ketoacidosis may occur

Question 25

types of insulin

Answer 25

i.	Numerous forms of rapid-acting, short-acting, intermediate-acting, long-acting, and a combination 
see p 690 antidiabetic insulins
1. rapid acting insulin
-lispro (humalog)
-aspart (novolog)
-glulisine (apidra)
2. short acting
-regular
3. intermediate acting
-isophane (NPH)
4. long acting
-glargine (lantus)
-detmir (levemir)

Question 26

rapid acting insulin

Answer 26

lispro(humalog)
aspart(novolog)
glulisine(apidra)
onset: 15-30 mins
peak: 30-90 mins
duration: 1-5 hrs

Question 27

short acting insulin

Answer 27

regular

onset: subq=30 mins, IV=15mins
peak: subq=2.5-5hr, IV=15-30min
duration: subq=4-12hrs, IV=30-60mins

Question 28

intermediate acting insulin

Answer 28

isophane (NPH)

onset: 1-2 hrs
peak: 6-12 hrs
duration: 18-24 hrs

Question 29

long acting insulin

Answer 29

glargine (lantus)
detmir (levemir)
onset: 1-1.5 hr
peak: none
duration: 24 hr

Question 30

insulin resistance

Answer 30

iii. Antibodies develop over time with animal insulin : slowing onset of insulin action and duration of action
iv. Obesity : causative factor for insulin resistance
v. Less allergens with human and regular insulin

Question 31

storage of insulin

Answer 31

i. Unopened vials must be refrigerated until needed
ii. May be kept at room temperature for 1 month or 3 months if left refrigerated
iii. Never place in the freezer or direct sunlight/high temperature area
iv. Prefilled syringes should be kept refrigerator and used within 1-2 weeks.

Question 32

sliding scale insulin coverage

Answer 32

i. Insulin can be administered in adjusted doses dependent on the patient’s blood glucose
ii. Sliding scale coverage provides more consistent blood glucose levels

Question 33

insulin pen injectors

Answer 33

i. Pen contains disposable needle with disposable prefilled pen
ii. Deliver more accurate dosing than traditional syringe and vial of insulin
iii. Considered more expensive: advantages outweigh increase in cost

Question 34

insulin pumps

Answer 34

i. Alternative to daily insulin injections
ii. Computerized devices with an insulin reservoir, and capability to deliver continuous insulin administration at varying times
iii. There are implantable and portable pumps available
iv. Provides basal dosing and bolus doses
v. Aids in reducing risk of hypoglycemic reactions and maintains glycemic control
vi. Must continue to monitor glucose at minimum of 4 times a day
vii. Most beneficial for Type 1 diabetics

Question 35

SE/ADV rxn

Answer 35

hypoglycemic rxn, somogyi effect, dawn phenomenon, diabetic ketoacidosis

Question 36

hypoglycemic rxn (insulin shock)

Answer 36

A. More insulin administered than needed for glucose metabolism
B. Nervousness, trembling, lack of coordination, cold and clammy skin, headaches: patient may be combative or incoherent
C. Treatment includes administering glucose
a. May give glucose orally if coherent and alert
b. Administer glucose IV if disoriented/unable to swallow

Question 37

somogyi effect

Answer 37

A. Hypoglycemic condition occurring in predawn hours of 2:00 AM to 4:00 AM
B. Rapid decrease in blood glucose during sleep: release of hormones to increase glucose by lipolysis, gluconeogenesis, and glycogenolysis
C. Results in hyperglycemia upon awakening
D. Treatment includes monitoring blood glucose between 2:00 AM and 4:00 AM, and reducing insulin at bedtime

Question 38

dawn phenomenon

Answer 38

A. Hyperglycemia on awakening d/t rise in BG and decreased levels of insulin
B. People with diabetes do not have normal insulin response to adjust
C. May cause headache, night sweats, and nightmares
D. Treatment includes increasing insulin administered at bedtime

Question 39

diabetic ketoacidosis (hyperglycemic reaction)

Answer 39

A. Inadequate amounts of insulin: sugar cannot be metabolized for energy> fat catabolism occurs > byproduct fatty acids (ketones) are used for energy causing ketoacidosis
a. Extreme thirst, polyuria, fruity odor of breath, kussmaul breathing (deep, rapid, labored, and distressed breathing), rapid but thready pulse, dry mucous membrane, and a blood sugar >250 mg/dL
C. Need to continuously monitor blood glucose, and may need to be on an insulin gtt (continuous IV infusion) with serial laboratory testing

Question 40

oral antidiabetic drugs (oral hypoglycemic drugs)

Answer 40

i. Should only be used in Type 2 diabetes- not for Type 1 diabetics (Type 2 diabetics still produce insulin from the pancreas)

Question 41

first and second generation sulfonylureas

Answer 41

oral antidiabetics
A. Chemically related to sulfonamides > no antibacterial activity
B. Stimulate pancreatic beta cells to secrete insulin > increases insulin cell receptors > increases availability of cells to bind insulin for glucose metabolism

Question 42

first generation sulfonylureas

Answer 42

a. Short-acting
b. Intermediate-acting
c. Long-acting

Question 43

second generation sulfonylureas

Answer 43

a. Increase tissue response to insulin > decrease glucose production by liver
b. Higher risk for hypoglycemia than 1st generations > lower dosing than 1st generation
c. Should not be used with kidney or liver dysfunction

Question 44

glipizide (Glucotrol, Glucotrol XL)

Answer 44

sulfonylurea
PT: hyperglycemia type II
PD: Directly stimulates beta cells in pancreas > secretes insulin > indirectly alters sensitivity of peripheral insulin receptors > increased insulin binding
2. Onset: 15-30 minutes
3. Peak: 1-2 hours
4. Duration: 12-24 hours
CI: diabetic ketoacidosis
PREC: Hep/renal dysfunction, elderly, debilitated/malnourished patients, adrenal/pituitary insufficiency
ADV: Hypoglycemia, tachycardia
2. Life threatening:
a. Agranulocytosis, leukopenia, thrombocytopenia
SE: n/d/anorexia/constipation/hunger, Drowsiness/headache/confusion/anxiety, visual disturbances
DFL: Alcohol: disulfiram-like reaction (flushing, headache, sweating, nausea, violent vomiting)
Altered LFTs
Green tea may potentiate hypoglycemia

Question 45

biguanides: metformin (glucophage)

Answer 45

non-sulfonylureas oral antidiabetic
A. Decreasing hepatic production of glucose from stored glycogen > diminishes increase in serum glucose after a meal > displaces effects of post-prandial hyperglycemia
B. Decreases absorption of glucose from small intestine > increases insulin receptor sensitivity, and peripheral glucose reuptake at cellular level
C. Does not produce hyper or hypo glycemia
D. Monotherapy can be effective > most commonly combined with sulfonylurea
E. Need to hold for 48 hours before receiving IV contrast > may induce lactic acidosis, or acute renal failure

Question 46

metformin, buganide (Glucophage, Glucophage XR)

Answer 46

non-sulfonylureas oral antidiabetic
PT: Control hyperglycemia in Type 2 diabetics
PD: Increases binding of insulin to receptors, improves tissue sensitivity to insulin, increases glucose transport to skeletal muscles and fatty tissues, decreases glucose production in liver > reducing gluconeogenesis, reduces intestinal glucose absorption
CI: Diabetic Ketoacidosis, radiographic contrast dye, current infection, renal dysfunction
PREC: Pregnancy/lactation, children, alcoholism, cardiopulmonary insufficiency, current infection, hepatic dysfunction
ADV: Lactic acidosis, vitamin B12 deficiency, palpitations, elevated liver enzymes, hypoglycemia, infection
ii. Life threatening: Lactic acidosis
SE: Dizziness, headache, fatigue, agitation, bitter or metallic taste, anorexia, weight loss, n/v/d, flushing
DFL: Altered LFTs, Green tea may potentiate hypoglycemia

Question 47

alpha-glucosidase inhibitors: acarbose (precose) and miglitol (glyset)

Answer 47

• Inhibit digestive enzyme (aflpha-glucosidase) in small intestine responsible for release of glucose from complex carbohydrates  delays absorption of complex carbohydrates

Question 48

acarbose (Precose)

Answer 48

alpha-glucosidase inhibitor

a. No systemic effects: not absorbed into the body in high amounts
b. Does not cause hypoglycemic reaction
c. Intended for patients in which diet alone is not effective

Question 49

miglitol (Glyset)

Answer 49

alpha-glucosidase inhibitor

a. Absorbed from the GI tract
b. Does not cause hypoglycemia unless taken with a sulfonylurea or insulin

Question 50

thiazolidinediones

Answer 50

A. Decrease insulin resistance and improve blood glucose control
B. Two drugs used for therapy
a. pioglitazone (Actos)
i. Can be combined with sulfonylurea or insulin
b. rosiglitazone (Avandia)
i. Can be combined with metformin
c. Both medications are contraindicated in class III & IV heart failure due to fluid retention
d. Neither medication will cause hypoglycemia if taken alone

Question 51

Repaglinide and nateglinide

Answer 51

short acting meglitinide oral antidiabetic drugs
B. Stimulate beta cells to release insulin
C. Work similarly to sulfonylurea’s
D. Can be used alone or in combination with metformin in patients with type 2 diabetes
E. Cannot be given to patient’s with liver dysfunction due to risk of decrease in liver metabolism >increased levels of drug in the body > risk for hypoglycemia

Question 52

Sitagliptin phosphate and saxagliptin

Answer 52

oral antidiabetic classified as incretin modifiers (below meglitinide oral antidiabetic) for treatment of type 2 diabetes
H. Increase level of incretin hormones, increase insulin secretion, and decrease glucagon secretion  reduce glucose production
I. Used as adjunct treatment with exercise and diet to reduce plasma glucose levels.

Question 53

NI for oral antidiabetics

Answer 53

A. Assess baseline vital signs
B. Potential for increased cardiac function and oxygen consumption > potential for cardiac dysrhythmias
C. Administer oral antidiabetics with food to decrease GI upset
D. Monitor blood glucose levels
a. 70-110 for serum glucose

Question 54

PT ED for oral antidiabetics

Answer 54

A. antidiabetics are not insulin, but may cause a hypoglycemic reaction, especially sulfonylureas
B. Teach s/s of hypoglycemia
(Headache, nervousness, sweating, tremors, rapid pulse) And hyperglycemia (Polyuria, polydipsia, and sweet, fruity breath odor)
D. Teach patient how to manage hypoglycemic episode
i. Glucagon if not responsive > 911
Complex carbohydrates if able to swallow and alert
E. There is a need for insulin in place of antidiabetic medications due to stress, illness/surgery, or infections
F. Importance to take the medication as prescribed, and to implement lifestyle changes including dietary changes
G. Wear a MedicAlert bracelet
H. Demonstrate return demonstration how to properly check blood sugar

Question 55

guidelines/criteria for oral antidiabetic therapy for type 2 diabetes

Answer 55

A.	Onset of diabetes at age 40 or older
B.	Diagnosis of diabetes <5 years
C.	Normal or over weight
D.	Fasting blood glucose <200
E.	<40 units of insulin/day
F.	Normal renal and hepatic function

Question 56

other antidiabetic agents

Answer 56

A. exenatide (Byetta)
B. liraglutide (Victoza)
xi. Improve beta-cell responsiveness > improves glucose control in type 2 diabetes
xii. Additionally, enhance insulin secretion, beta-cell responsiveness, glucagon suppression, slow gastric emptying, and reduce food intake
xiii. Not a substitute for insulin, and should not be used in type 1 diabetes, DKA, impaired renal function, or severe GI disease

Question 57

hyperglycemic drugs

Answer 57

glucagon, diazoxide

Question 58

glucagon

Answer 58

hyperglycemic drug
A. Hyperglycemia hormone secreted by alpha cells of islets of Langerhans
B. Increases blood sugar by stimulating glycogenolysis
a. Protects body cells > mostly brain and retina > provides nutrients, and energy to maintain body function
C. Glucagon is available for parenteral use (subq, IM, IV) to treat insulin-induced hypoglycemia
D. Example
a. If patient is semi or unconscious, and unable to take oral glucose, the alternative is parenteral
E. Those prone to hypoglycemic events should keep glucagon at home, and on the person in case of emergency
F. BG levels begin to increase within 10 min of administration

Question 59

diazoxide

Answer 59

A. Increases blood sugar by inhibiting insulin release from beta cells > stimulating release of epinephrine from adrenal medulla
B. Chemically related to thiazide diuretics
C. Not indicated for acute hypoglycemic reaction> used for hypoglycemia caused by hyperinsulinism
D. Long half-life, highly protein-bound with 1hr onset of action and 8-hour duration of action.