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NURS 424 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Type 1 DM

A

Age of onset: childhood and young adulthood

Cause: heredity, autoimmune response against insulin-producing beta cells

Endogenous insulin: secretion markedly diminished early in disease, can be totally absent later

Nutritional status: thin, catabolic state

Symptoms: polydipsia, polyphagia, polydipsia, fatigue, weight loss

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2
Q

Type 1 DM: treatment

A

Must include insulin

Diet and exercise help increase insulin sensitivity

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3
Q

Type 2 DM

A

Age of onset: adulthood

Cause: weight gain, age, inactivity, genetics

Endogenous insulin: low levels (insulin deficiency), normal, or high (insulin resistance)

Nutritional status: obesity common

Symptoms: asymptomatic; polydipsia or polyuria may be present

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4
Q

Type 2 DM: treatment

A

Combination of medications, diet, exercise, insulin

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5
Q

Insulin MOA (fivefold)

A

1) stimulates glucose entry into cells
2) increases storage of glucose as glycogen in muscle and liver cells
3) inhibits glucose production in liver and muscle cells
4) promotes protein synthesis by increasing amino acid transport into cells
5) enhances fat storage and prevents mobilization for fat for energy

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6
Q

Rapid-acting examples

A

Lispro (Humalog), aspart (NovoLog), glulisine (Apidra)

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7
Q

Rapid-acting: onset, peak, duration

A

Onset: 5 minutes
Peak: 1 hour
Duration: 4-5 hours

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8
Q

Short-acting examples

A

Regular (Humulin)

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9
Q

Short-acting: onset, peak, duration

A

Onset: 30-45 minutes before eating
Peak: 3-4 hours
Duration: 4-10 hours

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10
Q

Ideal BG parameters for fasting glucose and bedtime glucose

A

Fasting glucose: <126-130

Bedtime glucose: <140

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11
Q

Intermediate-acting examples

A

NPH

Looks cloudy and has to be mixed before its injected

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12
Q

Intermediate-acting: onset, peak, duration

A

Onset: 30 minutes - 1 hour
Peak: 4-10 hours
Duration: 12-24 hours

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13
Q

Long-acting examples

A

Glargine (Lantus), detemir (Levemir), degludec (Tresiba)

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14
Q

Long-acting: onset, peak, duration

A

Onset: 2-4 hours
Peak: peak less
Duration: 24 hours

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15
Q

Insulin: absorption

A

Abdominal site absorbs 50% more than other sites

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16
Q

Insulin: metabolism

A

Induces CYP1A2

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17
Q

Insulin: ADR

A

Hypoglycemia, diabetic ketoacidosis (breaks down muscle/fat for energy)

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18
Q

Insulin: patient education

A

Stop drinking alcohol –> increases hypoglycemia

Don’t take with beta blockers –> masks hypoglycemia symptoms (inhibit hepatic glucose production)

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19
Q

Which forms of insulin can pregnant women use?

A

Rapid and short-acting insulin (does not cross placenta)

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20
Q

How does hypothyroidism affect insulin production?

A

Delays insulin breakdown –> require less insulin units

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21
Q

How does hyperthyroidism affect insulin production?

A

Increases renal clearance –> require more insulin than baseline

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22
Q

What tests should be ordered to monitor insulin effectiveness?

A

Hgb A1C (glycohemoglobin), renal function (GFR), CBC

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23
Q

How often should A1C be drawn in patients who are meeting treatment goals and have stable glycemic control?

A

Twice a year

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24
Q

How often should A1C be drawn in patients whose treatment has changed/not meeting goals?

A

Quarterly

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25
Q

Insulin: contraindications

A

Hepatic dysfunction, renal impairment

Caution in pregnancy and hypo/hyperthyroidism

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26
Q

Glucagon: MOA

A

Accelerates liver glucogenolysis –> increased breakdown of glycogen to glucose and inhibition of glycogen synthesis –> elevated blood glucose levels

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27
Q

Glucagon: contraindications

A

Hypersensitivity to glucagon or lactose

Avoid in insulinoma or pheochromocytoma

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28
Q

Metformin: classification

A

Biguanides

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29
Q

Metformin: MOA

A

Increases peripheral glucose uptake and utilization –> improve insulin sensitivity

Decreases hepatic glucose production and intestinal absorption of glucose

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30
Q

Metformin: patient education

A

Does NOT stimulate insulin release, does NOT cause hypoglycemia

Lowers postprandial and basal plasma glucose levels

Hold 48 hours before and after radiologic studies with contrast

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31
Q

Metformin: contraindications

A

Avoid with GFR <30 (caution with GFR 30-45, requires close monitoring)

Liver disease

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32
Q

True/False

Metformin is first-line therapy in pregnancy

A

False

Insulin is first line therapy, but Metformin can be considered by OB

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33
Q

Metformin: ADR

A

Lactic acidosis (death, hypothermia, HTN, resistance of bradyrhythmias)

N/D, bloating, flatulence, HA, vitamin B12 deficiency

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34
Q

Which classification of diabetic medication would you prescribe for someone with tissue insensitivity to insulin?

A

Biguanides (ex Metformin), thiazolidinediones

Improve insulin sensitivity

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35
Q

Pioglitazone (Actos): classification

A

Thiazolidinediones (TZD)

36
Q

Pioglitazone (Actos): MOA

A

Enhances insulin sensitivity by improved insulin action in the cell –> increases utilization of available insulin by the liver and muscle cells

Decreases hepatic glucose production

37
Q

Pioglitazone (Actos): patient education

A

Does NOT cause hypoglycemia, increased bone fracture risk

Avoid in pregnancy, lactation, and children younger than 18 years

38
Q

Pioglitazone (Actos): contraindications

A

Avoid in NYHA class III and IV HF, patients with ALT >2.5, active or history of bladder cancer

39
Q

Pioglitazone (Actos): ADR

A

Fluid retention, weight gain, HA, myalgia, HTN, URI

40
Q

Which classification of diabetic medication would you prescribe for someone with insufficient production of endogenous insulin?

A

Sulfonylureas - cause an increase in insulin production

41
Q

Glipizide, glyburide, glimepiride: classification

A

Sulfonylureas

42
Q

Glipizide, glyburide, glimepiride: MOA

A

Increases endogenous insulin secretion by beta cells

Reduce glucose release from liver

43
Q

Glipizide, glyburide, glimepiride: contraindications

A

Avoid in elderly d/t hypoglycemia, in pregnancy/lactation and children, sulfa allergies, G6PD deficiency

Caution in renal and hepatic impairment

44
Q

Glipizide, glyburide, glimepiride: ADR

A

Hypoglycemia, weight gain, nausea, epigastric fullness, heartburn, rashes, pruritus, urticaria, agranulocytosis

45
Q

Repaglinide (Prandin), nateglinide (Starlix): classification

A

Meglitinides

46
Q

Which classification of diabetic medication would you prescribe for someone with an impaired response of beta cells?

A

Meglitinides - increases secretion of insulin

47
Q

Repaglinide (Prandin), nateglinide (Starlix): MOA

A

Blocks ATP-dependent K channels, depolarizing the membrane and facilitates calcium entry through calcium channels

Increased calcium stimulates insulin release from beta cells

48
Q

True/False
Short-acting insulin secretagogues (aka meglitinides) are the most effective agent at reducing postprandial blood glucose levels

A

True

49
Q

Repaglinide (Prandin), nateglinide (Starlix): patient education

A

Take 30 minutes before meal

If skipped meal, skip dose

50
Q

Repaglinide (Prandin), nateglinide (Starlix): contraindication

A

Avoid in elderly d/t hypoglycemia, pregnancy/lactation and children

Caution in renal and hepatic impairment

51
Q

Repaglinide (Prandin), nateglinide (Starlix): ADR

A

Hypoglycemia, weight gain, HA, diarrhea, arthralgia, chest or back pain

52
Q

Acarbose: classification

A

Alpha-glucosidase inhibitor

53
Q

Which classification of diabetic medication would you prescribe for someone with excessive production of glucose by the liver?

A

Alpha-glucosidase inhibitors - inhibit absorption of carbohydrate in GI tract (starch busters)

ALSO, metformin: improves hepatic response to elevated blood gas, decreases glucose production, and decrease GI absorption

54
Q

Acarbose: MOA

A

Competitively inhibits absorption of complex carbohydrates from small bowel –> delays glucose absorption

55
Q

Acarbose: ADR

A

Flatulence, diarrhea, abdominal pain, elevated serum transaminases

56
Q

Acarbose: patient education

A

Difficult to tolerate d/t GI upset, typically an add-on to current therapy

Works best for postprandial glucose elevation

57
Q

Acarbose: contraindication

A

Avoid in bowel disease , predisposed to intestinal obstruction, pregnancy and lactation

Caution in renal and hepatic impairment

58
Q

True/False

Alpha-glucosidase inhibitors cause hypoglycemia

A

False

59
Q

-flozins: classification

A

Selective sodium-glucose cotransporter 2 inhibitors (SGLT-2)

60
Q

SGLT-2: MOA

A

Inhibits renal SGLT-2 in proximal tubule, blocks reabsorption of glucose in kidneys –> increased urinary glucose excretion and reduction of plasma glucose

61
Q

SGLT-2: ADR

A

Hyperkalemia, GU fungal infection, UTI, renal insufficiency, urinary frequency, hypotension, urticaria

62
Q

SGLT-2: patient education

A

Urinary frequency and hypotension caused by volume depletion

Can cause weight loss, evidence of reducing ASCVD risk

Add-on to current therapy

63
Q

SGLT-2: contraindication

A

BLACK BOX: risk of Fournier’s gangrene

Avoid in GFR <30 (dose reduce if <60), pregnancy and lactation

64
Q

SGLT-2: patient education

A

Increased risk for bone fractures, fall risk d/t hypovolemia

65
Q

Which classification of diabetic medication would you prescribe for someone with impaired GLP-1 activity (rapid intestinal glucose dumping)?

A

Depeptidyl peptidase 4 (DPP-4) slow inactivation

66
Q

-gliptins: classification

A

DPP-4

67
Q

DPP-4: MOA

A

Inhibits DPP-4 enzyme, resulting in prolonged incretin (GLP-1 and GIP) hormone levels

68
Q

DPP-4: contraindications

A

Avoid in pregnancy and lactation

Caution in renal impairment (except linagliptin)

69
Q

DPP-4: ADR

A

Hypersensitivity reactions, acute pancreatitis, arthralgia, hypoglycemia

70
Q

-tides: classification

A

GLP-1

71
Q

GLP-1 (-tides): MOA

A

Analog of incretin hormone GLP-1 which increases glucose dependent insulin secretion, decreases inappropriate glucagon secretion, slows gastric emptying

72
Q

GLP-1 (-tides): ADR

A

N/V/D, injection site reaction, HA

73
Q

GLP-1 (-tides): patient education

A

Promotes satiety and weight loss

74
Q

GLP-1 (-tides): contraindications

A

Avoid in moderate to end stage renal disease, patients with severe GI disease

BLACK BOX: risk of thyroid c-cell tumors

75
Q

Levothyroxine (Synthroid): MOA

A

Synthetic form of T4 - endogenous hormone secreted by thyroid gland (T4 converts to T3)

Bind to thyroid receptor proteins in cell nucleus and exert metabolic effects through control of DNA transcription and protein synthesis

76
Q

Levothyroxine (Synthroid): patient education

A

Given on an empty stomach (30 minutes prior to meals) in morning

Takes 6-8 weeks to reach steady state

77
Q

Levothyroxine (Synthroid): contraindications

A

Avoid after recent MI

Caution in patients with CVD, adrenal insufficiency

78
Q

Levothyroxine (Synthroid): ADR

A

Tachycardia, HTN, anxiety, nervousness, insomnia, weight loss

79
Q

Methimazole (Tapazole): MOA

A

Inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland

Does NOT inactivate circulating T3 and T4

80
Q

Methimazole (Tapazole): ADR

A

Drowsiness, HA, arthralgia, skin rash, urticaria, fever, agranulocytosis, hepatitis

81
Q

Methimazole (Tapazole): contraindication

A

Avoid in first trimester of pregnancy, use in lowest dose in lactation

Caution with other meds that suppress bone marrow

82
Q

Methimazole (Tapazole): patient education

A

Long half-life and no risk for hepatic toxicity –> preferred over PTU

Take PTU during first trimester, then start methimazole once second trimester occurs

83
Q

PTU: MOA

A

Inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland

Blocks conversion of T4 to T3 in peripheral tissue (dose NOT inactivate circulating T3 and T4)

84
Q

PTU: ADR

A

Drowsiness, HA, arthralgia, skin rash, urticaria, fever, agranulocytosis, hepatitis

85
Q

PTU: contraindications

A

BLACK BOX: hepatotoxicity

Avoid in pediatrics; lowest dose in lactation

Use cautiously with other meds that cause bone marrow suppression

86
Q

PTU: patient education

A

Increased bleeding risk

NURS 424 (35 decks)

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