AntiDiabetic Drugs Flashcards

1
Q

Decreases insulin release; increases glucose output from liver and muscles; increases breakdown of fat to Free Fatty Acids

A

Catecholamines

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1
Q

From beta cells of the pancreas; Decreases blood glucose; glycogen storage;
adipose tissue deposit; synthesis of proteins to form amino acids

A

Insulin

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1
Q

From alpha cells of the pancreas;
Increases blood glucose

A

Glucagon

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1
Q

Increases insulin release; decreases glucagon release; stimulates satiety center; slows GI emptying

A

Incretins

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2
Q

Increases glucose output; decreases insulin sensitivity

A

Corticosteroids

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3
Q

Type __ diabetes is common in
younger people and is connected
with cases of destruction of beta
cells of the pancreas.

A

1

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4
Q

*Type _ is adult-onset and is
associated with not enough insulin
to maintain glucose control.

A

2

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5
Q

results when there is an increase in
glucose in the blood.

*Clinical signs and symptoms include
fatigue, lethargy, irritation, glycosuria,
polyuria, polyphagia, polydipsia, and
itchy skin (from the accumulation of
wastes that liver cannot clear).

A

Hyperglycemia (high blood sugar)

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6
Q
  • If unchecked, it can lead to ____ showing fruity breath from ketons excreted
    through the lungs, slow, deep respirations
    (Kussmaul respiration) & loss of orientation and
    coma.
A

Diabetic ketoacidosis (DKA)

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7
Q

___ is a blood glucose
concentration lower than 40 mg/dL
and can occur in many clinical situations like starvation and overtreatment of hyperglycemia.
Manifestations include headache, paresthesias (numbness), hunger, and diaphoresis (sweating).

A

Hypoglycemia

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8
Q

a drug that is used to control
glucose in patients with diabetes mellitus.

  • It is the only parenteral antidiabetic
    agent available for exogenous
    replacement of low levels of insulin
A

insulin

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9
Q

Indications
* Treatment of type 1 diabetes
* Treatment of type 2 diabetes
when other agents have failed
* Short-term treatment of type
2 diabetes during periods of stress
* Management of diabetic
ketoacidosis, hyperkalemia,

A

insulin

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10
Q

Insulin does enter breast milk but it
is destroyed in the GI tract and does
not affect the nursing infant

A

Insulin does enter breast milk but it
is destroyed in the GI tract and does
not affect the nursing infant

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11
Q

Adverse Effects

*hypoglycemia and ketoacidosis
* local reactions at the injection site
lipodystrophy (due to injecting cold insulin)

A

Insulin

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12
Q

nursing consideration in injecting insulin

A
  • avoid vigorous shaking to ensure uniform
    suspension of insulin
  • Distance of rotations should be at least 1 inch or 2.54cm
  • Do not inject in the 2-inch radius around the umbilicus
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13
Q

only intravenous (IV) insulin is ___

A

Regular insulin

14
Q

stimulate insulin release
from the beta cells in pancreas. They
improve insulin binding to insulin
receptors and may actually increase
the number of insulin receptors.

  • These drugs are only effective in
    patients who have functioning beta
    cells.
A

Sulfonylureas

15
Q

Indications
* used as adjunct to diet and exercise for
the treatment of type 2 diabetes older
than 10 years of age; extended release
form for patients older than 17 years of
age;

A

Sulfonylureas

15
Q

___ generation sulfonylureas
* safer for patients with renal dysfunction as
they are excreted in urine and bile,
* absence of interaction to many protein-
bound drugs, and longer duration of action.

A

2nd

16
Q

___ generation sulfonylureas

declining as more effective drugs
* thought to possibly cause an increase in
cardiovascular death.

A

1st

17
Q

Antidiabetic drugs are a group of
drug structurally unrelated to
sulfonylureas and are effective when
used in combination with insulin or
sulfonylureas.

A

Other Oral Hypoglycemic Agents (OHA)

18
Q

Other Oral Hypoglycemic Agents (OHA)/ Antidiabetic Agents

*Alpha-glucosidase inhibitors
* Biguanide
*Meglitinides
* Synthetic human amylin
* Incretin mimetics
*DPP-4 inhibitors

A

Other Oral Hypoglycemic Agents (OHA)/ Antidiabetic Agents

*Alpha-glucosidase inhibitors
* Biguanide
*Meglitinides
* Synthetic human amylin
* Incretin mimetics
*DPP-4 inhibitors

19
Q
  • E.g. Acarbose and Miglitol
  • inhibit alpha-glucosidase, an enzyme that
    breaks down glucose for absorption.
    Therefore, they delay the absorption of
    glucose.
  • They have only a mild effect on glucose
    levels and do not enhance insulin
    secretion.
  • They are associated with severe hepatic
    toxicity and GI distress.
A

Alpha-glucosidase inhibitors

20
Q
  • E.g. Metformin
  • decrease the production and increases
    the uptake of glucose.
  • effective in lowering blood glucose and
    [does not cause hypoglycemia as the
    sulfonylureas do.]
  • It has been associated with
    development of lactic acidosis and GI
    distress.
A

Biguanide

21
Q
  • E.g. Pramlintide
  • works to modulate gastric emptying after a
    meal to cause a feeling of fullness or satiety.
  • prevents the postmeal rise (SUGAR RUSH) in glucagon that
    usually elevates glucose levels.
  • Human amylin is a hormone produced by
    beta cells in the pancreas that is important
    in regulating postmeal glucose levels.
  • It should not be used when patient is unable
    to eat.
A

Synthetic human amylin

21
Q

E.g. Nateglinide and Repaglinide
* are newer agents that act like
sulfonylureas to increase insulin
release.

A

Meglitinides

21
Q
  • E.g. Exenatide and Liraglutide
  • mimic the effects of GLP-1(enzyme that breakdown protein): enhancement of glucose-dependent insulin secretion by the beta cells in
    the pancreas
  • depression of elevated glucagon
    secretion, and slowed gastric emptying
    to help moderate and lower blood
    glucose levels.
A

Incretin mimetics

21
Q
  • lina-, saxa-, and sitagliptin
  • slow the breakdown of GLP-1 to
    prolong the effects of increased
    insulin secretion, decreased
    glucagon secretion, and slowed GI
    emptying.
A

DPP-4 inhibitors