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Pharmacology for Advanced Practice Nurses > Endocrine Deck 3 > Flashcards

Endocrine Deck 3 Flashcards

1
Q

GLP-1 Agonists examples

A

Exenatide (Byetta) and others

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2
Q

GLP-1 Agonists pharmacodynamics

A

Promote insulin release from pancreatic beta cells in the presence of elevated glucose
Mimic natural incretins
Slow glucose absorption from gut; promote satiety
Slow postparandial spikes

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3
Q

GLP-1 Agonists precautions and contraindications

A

Acute pancreatitis noted in post-marketing surveillance
Severe GI disease (colitis, Crohn’s disease)
Pregnancy (check with specialists)

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4
Q

GLP-1 Agonists drug interacions

A

Increased international normalized ratio (INR) if administered with warfarin
Digoxin

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5
Q

GLP-1 Agonists Clinical use only for type 2 DM

A

Add-on therapy is typical
Combine with:
Metformin, sulfonylurea, others

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6
Q

GLP-1 Agonists monitoring

A

Glycemic control and GI distress

Potential site reactions

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7
Q

GLP-1 Agonists patient education

A

Administration of subcutaneous (SC) injection for rapid release
60 minutes before meals
Dosed 6 hours apart
If dose is missed, wait for next scheduled time

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8
Q

GLP-1 Agonists ADR

A

GI upset/nausea (major cause of noncompliance)

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9
Q

GLP-1 Agonists are

A

injectable and add on therapy, work on incretins and how they act.

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10
Q

GLP-1 Agonists

Extended-release forms

A

weekly injections

Works as well or better than rapid release on HgA1C and weight

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11
Q

GLP-1 Agonists ER GI issues are

A

GI issues more transient

Rapid and extended release have different impacts on postprandial vs fasting glucose levels

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12
Q

SGLT-2 Inhibitors examples

A

Canaglilozin, dapagliflozin

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13
Q

SGLT-2 Inhibitors MOA

A

Reduce blood glucose by blocking reabsorption of glucose in kidney
Also reduce BP and can lead to mild weight loss

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14
Q

SGLT-2 Inhibitors first choice to add

A

if HgA1C is not at goal with metformin due to significant reduction of CV risk and progression of renal functional loss

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15
Q

SGLT-2 Inhibitors can cause

A

Can cause genital yeast infections which can trigger the rare Fournier’s gangrene

if it happens take them off

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16
Q

SGLT-2 Inhibitors sometimes linked to

A

Sometimes linked with increased K+, bladder cancer and increased lipid levels

do CMP and urinalysis

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17
Q

Glucagon is considered

A

an insulin antidote: used in patients with diabetes who experience hypoglycemia or insulin overdose

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18
Q

Glucagon Pharmacodynamics

A

Glucagon stimulates hepatic gluconeogenesis and glycogenolysis, raising BG levels.
BG concentration rises within 10 minutes of injection, and maximal concentrations are attained at approximately a half hour after injection.
Hepatic stores of glycogen are necessary for glucagon to produce an anti-hypoglycemic effect.

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19
Q

Glucagon Pharmacokinetics

A

Well absorbed after parenteral administration

Extensively metabolized by the liver and kidneys

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20
Q

Glucagon

Precautions and contraindications

A

May be used with pregnant women and children

Administered cautiously to patients suspected of having pheochromocytoma or insulinoma

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21
Q

Glucagon ADR

A

nausea and vomiting, allergic reactions

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22
Q

Glucagon

A

Drug interaction

23
Q

Glucagon Clinical use and dosing

A

Reversal of hypoglycemia; prevention of low sugars for colonoscopy after 3-day preparations

24
Q

Glucogon dose

A

In primary care setting: intramuscular (IM) dosing
Less than 20 kg weight: 0.5 mg or 20 to 30 mcg/kg/dose, repeat every 20 minutes
Less than 20 kg weight: adult dosing 1 mg/IM, may repeat in 20 minutes

25
Q

Glucagon monitoring and patient education

A

Monitoring: BG levels immediately prior to and after injection

Patient education
Administration
Educate family members and roommates on how to test BG and how to administer IM glucagon.

26
Q

Glucagon depletes

A

glycogen stores; patient should be given supplemental carbohydrates as soon as he or she awakens and is able to swallow, especially children or adolescents.

27
Q

Drugs affecting the hypothalamus-pituitary-adrenal (HPA) axis–endocrine system

A

Bisphosphonates (covered later in the course)
Hypothalamic and pituitary hormones
Thyroid and antithyroid agents
Reproductive hormones (covered later in the course)
Corticosteroid-related hormones (covered later in the course)

28
Q

Human Growth Hormone name

A

Somatropin (genotropin)

29
Q

Somatropin MOA

A

Recombinant DNA technology is true human factor

Stimulates the growth and metabolism of nearly every cell in the body

30
Q

Somatropin Uses

A

short stature with or without normal GH levels

31
Q

Somatropin contraindicated in

A

patients with closed epiphyses (don’t used after finished growing)

32
Q

Somatropin dosing

A

highly individualized on the basis of child’s growth rate and anticipated trajectory of genetic height

33
Q

Somatropin pharmacodynamics

A

Initially there is insulin-like effect
Simulates growth of linear bones, skeletal muscles, and organs
Stimulates erythropoietin

34
Q

Erythropoietin is a

A

hormone that is produced predominantly by specialised cells in the kidney. Once it is made, it acts on red blood cells to protect them against destruction. At the same time it stimulates stem cells of the bone marrow to increase the production of red blood cells.

35
Q

Human Growth Hormone pharmacokinieitcs

A

intramuscular (IM) and subcutaneous (SC) drugs well-absorbed
Metabolism: hepatic, renal 90%
Excretion: renal

36
Q

Human Growth Hormone

Adverse drug reactions (ADRs)

A

Antibody development
Hyperglycemia, edema
Hypothyroidism
Arthralgia, headache, dizziness, flu-like symptoms

37
Q

Human Growth Hormone patient education

A

Pediatric administration: total weekly dose (0.16 to 0.24 mg/kg) divided into 6 to 7 doses
ADRs
Lifestyle management and need to prevent abuse

38
Q

HGH rational drug selection

A

NOT initiated by nurse practitioner in primary care practice; work with endocrinologist

39
Q

HGH Monitoring

A

Hepatic/renal function: before and during treatment

TSH, glucose, glycohemoglobin, based on symptoms and prior illnesses

40
Q

Thyroid hormones

A

Levothyroxine (T4), liothyronine (T3), and liotrix (a 4:1 mixture of T4 and T3)

41
Q

Thyroid hormones produce the

A

same effects in the body as endogenous thyroid hormones.

42
Q

Thyroid hormones also produce a

A

negative feedback loop to reduce further secretion of TSH and thyroid hormones.

43
Q

t4 is the drug of choice for

A

thyroid replacement and suppression therapy because of its longer half-life

44
Q

When do you take thyroid hormones

A

first thing in the morning on an empty stomach. Because they do not play with with other medications

45
Q

Thyroid hormone absorption

A

Absorption: oral – erratic 40% to 80%; decreased by age, food, health of gastrointestinal (GI) tract; greater than 99% is protein bound

46
Q

Thyroid hormone metabolism

A

liver, T4 is converted to T3 in the body; T4 produces both hormones

47
Q

Thyroid hromone excreted

A

bile/feces

48
Q

Thyroid Hormones

Precautions and contraindications

A

Contraindicated after acute myocardial infarction or thyrotoxicosis

49
Q

Thyroid Hormones

Pregnancy risk

A

factor A, and safe with children

50
Q

Thyroid hormones replacement is advised for

A

all pregnant women

51
Q

thyroid hormone increased metabolic rate

A

during pregnancy may require higher dosing from baseline.

52
Q

thyroid hormone is minimally

A

excreted in breast milk.

53
Q

children with hypothyroidism

A

need treatment

Pharmacology for Advanced Practice Nurses (50 decks)

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