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NR565 - Advanced Pharmacology > Week 5 - Peer support > Flashcards

Week 5 - Peer support Flashcards

1
Q

What is the primary defect in type 1 diabetes?

A

Destruction of pancreatic β cells—the cells responsible for insulin synthesis and release into the bloodstream.

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2
Q

The symptoms of type 2 diabetes result from what?

A

usually result from a combination of insulin resistance and impaired insulin secretion.

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3
Q

What is gestational diabetes

A

diabetes that appears in the pregnant patient during pregnancy and then subsides rapidly after delivery.

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4
Q

How should gestational diabetes be managed?

A

discontinue the oral drug and switch to insulin.

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5
Q

How do we diagnose diabetes?

A

Fasting plasma glucose ≥126 mg/dL

OR

Random plasma glucose ≥ 200 mg/dLplussymptoms of diabetes

OR

Oral glucose tolerance test (OGTT): 2-h plasma glucose ≥200 mg/dL or Hemoglobin A1c6.5% or higher

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6
Q

Is a fasting blood glucose of 125 consistent with pre-diabetes or diabetes?

A

Pre diabetes

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7
Q

What is a hemoglobin A1C of 5.7?

A

pre diabetes

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8
Q

What is a hemoglobin A1C of 6.7?

A

Diabetes

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9
Q

A random plasma glucose of ____ is suggestive of diabetes.

A

200 or more

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10
Q

What are the “classic” signs of diabetes?

A

polyuria, polydipsia, and unexplained weight loss.Ketonuria may also be present, but only if blood glucose is extremely high.

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11
Q

What are the Glycemic Treatment Targets for someone with diabetes?

A

A1c<7.0%
Pre meal plasma glucose 70–130 mg/dL
Peak post meal plasma glucose<180 mg/dL

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12
Q

How often should an A1c be drawn for someone with a initial A1c >7?

A

A1cshould be measured every 3 months until the value drops to 7% and at least every 6 months thereafter.

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13
Q

What are the three ways that insulin deficiency promotes hyperglycemia?

A

(1) increased glycogenolysis,
(2) increased gluconeogenesis
(3) reduced glucose utilization.

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14
Q

When drawing two insulins into one syringe, which insulin should be drawn up first Humulin R or Humulin N?

A

Humulin R, clear before cloudy or calm before the storm

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15
Q

What is the expected onset of Aspart (Novolog)?

A

10-20 min

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16
Q

What is the expected onset of Regular (Humulin R, Novolin R)?

A

30-60 min

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17
Q

What is the expected onset of NPH (Humulin N, Novolin N)?

A

60-120 min

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18
Q

What is the expected onset of Insulin glargine (U-100)?

A

70 min

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19
Q

Within how many minutes of a meal should Insulin Lispro (Humalog) be administered?

A

SubQ inj:within 15 min before or just after meals

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20
Q

When might insulin needs increase?

A

infection, stress, obesity, the adolescent growth spurt, and pregnancy after the first trimester.

Conversely, insulin needs aredecreasedby exercise and during the first trimester of pregnancy.

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21
Q

What are some things that may results in hypoglycemia?

A

Imbalance between insulin levels and insulin needs can also result from reduced intake of food, vomiting and diarrhea (which reduce absorption of nutrients), excessive consumption of alcohol (which promotes hypoglycemia), unusually intense exercise (which promotes cellular glucose uptake and metabolism), and childbirth (which reduces insulin requirements).

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22
Q

We need to educate our patients with diabetes on the signs and symptoms of hypoglycemia, what are they?

A
  • tachycardia
  • palpitations
  • sweating
  • nervousness.

However, if glucose declinesgradually,symptoms may be limited to those of CNS origin. Mild CNS symptoms include headache, confusion, drowsiness, and fatigue. If hypoglycemia is severe, convulsions, coma, and death may follow.

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23
Q

What medication might mask the signs of hypoglycemia?

A

Beta blockers

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24
Q

A BG less than what is considered hypoglycemia?

A

<70

Can be caused by
- excessive consumption of alcohol (which promotes hypoglycemia),
- unusually intense exercise (which promotes cellular glucose uptake and metabolism),
- childbirth (which reduces insulin requirements).

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25
Q

What is the MOA of Metformin?

A

Decreases glucose production by the liver, increases tissue response to insulin

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26
Q

What are the common adverse effects of Metformin?

A

Gastrointestinal (GI) symptoms: decreased appetite, nausea, diarrhea

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27
Q

What is black-box warning for Metformin and what are the signs?

A

Lactic acidosis

early signs of lactic acidosis include:
- hyperventilation
- myalgia
- malaise
- unusual somnolence

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28
Q

Is Metformin a good choice for patients who skip meals?

A

Yes, Metformin is well suited for patients who tend to skip meals.

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29
Q

Besides diabetes what is Metformin used to treat?

A

PCOS

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30
Q

What kind of deficiency are patients who are taking Metformin at risk for?

A

Metformin decreases absorption of vitamin B12 and folic acid and can thereby cause deficiencies of both.

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31
Q

Is Metformin a good option for patients with Heart Failure?

A

Because heart failure (HF) can predispose to lactic acidosis, metformin is contraindicated for people with failing hearts

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32
Q

Is Metformin or sulfonylureas more likely to significantly drop a patients blood sugar?

A

sulfonylureas

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33
Q

What is first-line treatment for a new diagnosis of diabetes type 2?

A

Lifetstyle changes + Metformin

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34
Q

What is the MOA of Sulfonylureas and Meglitinides (Glinides)?

A

Promote insulin secretion by the pancreas

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35
Q

How effective are Sulfonylureas in treating type 1 diabetes?

A

These drugs are of no help to patients with type 1 diabetes.

36
Q

What is the most important education to provide regarding sulfonylureas?

A

Educate patients about signs and symptoms of hypoglycemia.

37
Q

What is the MOA of Thiazolidinediones (Glitazones)?

A

Decrease insulin resistance and thereby increase glucose uptake by muscle and adipose tissue and decrease glucose production by the liver

38
Q

Which oral hypoglycemic is associated with heart failure?

A

Pioglitazone is associated withheart failure(HF) secondary to renalretention of fluid.If HF is diagnosed, pioglitazone should be discontinued or used in reduced dosage.

39
Q

What are the common adverse effects of -glucosidase inhibitors—acarbose?

A

Flatulence, cramps, abdominal distention, borborygmus (rumbling bowel sounds), anddiarrhea.

Acarbose can decrease absorption of iron, thereby posing a risk foranemia.

Hypoglycemiadoes not occur with acarbose alone but may develop when acarbose is combined withinsulinor asulfonylurea.

Liver dysfunction.

40
Q

What is the MOA of Dipeptidyl Peptidase-4 (DPP-4) Inhibitors (Gliptins)?

A

Enhance the activity of incretins (by inhibiting their breakdown by DPP-4) and thereby increase insulin release, reduce glucagon release, and decrease hepatic glucose production.

41
Q

Which patient population should we be cautious of when prescribing a DPP-4 inhibitor?

A

Use with caution in patients that have a history of pancreatitis.

42
Q

What is the MOA of Sodium-Glucose Cotransporter 2 (SGLT-2) Inhibitors?

A

Increase glucose excretion via the urine by inhibiting SGLT-2 in the kidney tubules, decreasing glucose levels and inducing weight loss by caloric loss through the urine. Good for HF.

43
Q

What are the most common adverse effects of Canagliflozin?

A
  • female genital fungal infections
  • urinary tract infections
  • increased urination.

Diuretic effect, the risk for dehydration and hypotension may be increased when used in combination with thiazide and loop diuretics.

44
Q

How do Glucagon-like peptide-1 receptor agonist (Byetta, Victoza, Trulicity) work to decrease blood sugar levels?

A
  • slow gastric emptying,
  • stimulate glucose-dependent release of insulin, - inhibit postprandial release of glucagon
  • suppress appetite.
45
Q

What is the most common side effect of Byetta?

A

GI effects—nausea, vomiting, and diarrhea—are common with exenatide (Byetta).

46
Q

Exenatide poses a risk for_______ and ________.

A

pancreatitis and renal impairment

47
Q

For a new diagnosis of diabetes, insulin should be started if the A1c is greater than what?

A

10

48
Q

What is the typical starting insulin dose?

A

Patients should be started on 10 IU

49
Q

How do we calculate a weight based starting insulin dose?

A

0.1-0.2 IU/kg a day (basal)

50
Q

In regards to total daily dose ___% is basal insulin and ___% is bolus (meal coverage) insulin.

A

​Total daily insulin dose (TDD) calculation includes basal insulin replacement and bolus insulin replacement. 50 and 50

51
Q

If the TSH was > ____ it would be suggestive of hypothyroidism.

A

6

52
Q

What is a normal TSH?

A

0.3–6

53
Q

What are the causes of hypothyroidism?

A

In iodine-sufficient countries, the principal cause ischronic autoimmune thyroiditis(Hashimoto thyroiditis).

Other causes are:

  • insufficient iodine in the diet
  • surgical removal of the thyroid
  • destruction of the thyroid by radioactive iodine.

Adult hypothyroidism may also result from insufficient secretion of TSH and TRH.

54
Q

When is treatment complete and a patient can discontinue taking medication for hypothyroidism?

A

In almost all cases, treatment must continue lifelong.

55
Q

Is medication for hypothyroidism safe in pregnancy?

A

Some authorities currently recommend routine screening for hypothyroidism as soon as pregnancy is confirmed. If hypothyroidism is diagnosed, replacement therapy should begin immediately. Maternal hypothyroidism can result in permanent neuropsychological deficits in the child.

56
Q

Biguanide MOA

A

Decreases glucose production by the liver, increases tissue response to insulin.

57
Q

MOA Second Generation Sulfonylureas/Meglitinides (Glinides)

A

Promote insulin secretion by the pancreas.

58
Q

MOA Thiazolidinediones (Glitazones)

A

Decrease insulin resistance and thereby increase glucose uptake by muscle and adipose tissue and decrease glucose production by the liver.

59
Q

MOA Dipeptidyl Peptidase-4 (DPP-4) Inhibitors (Gliptins)

A

Enhance the activity of incretins (by inhibiting their breakdown by DPP-4) and thereby increase insulin release, reduce glucagon release, and decrease glucose production by the liver.

60
Q

MOA Sodium-Glucose Cotransporter 2 (SGLT-2) Inhibitors

A

Increase glucose excretion via the urine by inhibiting SGLT-2 in the kidney tubules, decreasing glucose levels and inducing weight loss by caloric loss through the urine.

61
Q

MOA Glucagon-like Peptide-1 (GLP-1) Receptor Agonists (Incretin Mimetics)

A

Lower blood glucose by slowing gastric emptying, stimulating glucose-dependent insulin release, suppressing postprandial glucagon release, and reducing appetite.

62
Q

What would we expect the T3, T4 levels to be with hypothyroidism?

A

increased TSH, decreased T3, T4

63
Q

What are some s/s of hypothyroidism?

A

face is pale, puffy, and expressionless. The skin is cold and dry. The hair is brittle, and hair loss occurs. Heart rate and temperature are lowered. The patient may complain of lethargy, fatigue, and intolerance to cold. Mentation may be impaired

64
Q

What is the first-line drug for hypothyroidism?

A

Synthroid (levothyroxine)

65
Q

What is the average daily dose of synthroid/levothyroxine?

A

100–125 µg for 70 kg adult. Older adults have lower starting doses of 25–50 µg daily

66
Q

How should we advise our patients to take levothyroxine/synthroid?

A

on an empty stomach in the morning, at least 30 to 60 minutes before breakfast

67
Q

What are some drugs that reduce the absorption of the hypothyroid medication?

A
  • Histamine 2 (H2) receptor blockers (e.g., cimetidine [Tagamet]),
  • Proton pump inhibitors (e.g., lansoprazole [Prevacid]),
  • Sucralfate (Carafate),
  • Cholestyramine (Questran),
  • Colestipol (Colestid),
  • Aluminum-containing antacids (e.g., Maalox, Mylanta),
  • Calcium supplements (e.g., Tums, Os-Cal),
  • Iron supplements (e.g., ferrous sulfate), - - - - - Magnesium salts, Orlistat (Xenical)
68
Q

What drugs accelerate metabolism of hypothyroid meds?

A
  • phenytoin (Dilantin),
  • carbamazepine (Tegretol,
  • Carbatrol),
  • rifampin (Rifadin),
  • sertraline (Zoloft),
  • phenobarbital.
69
Q

When should we recheck TSH after initiation of Tx?

A

Check TSH 6-8 weeks after initiating therapy and after any dosage change

70
Q

Are levothyroxine products interchangeable?

A

Maintain patients on the same brand-name levothyroxine product. If changed recheck in 6 weeks. Advise patients to check with their prescriber before allowing a pharmacist to switch to a different levothyroxine product.

71
Q

What are some potential adverse effects of levothyroxine?

A

With an acute overdose,thyrotoxicosismay result.

Signs and symptoms include tachycardia, angina, tremor, nervousness, insomnia, hyperthermia, heat intolerance, and sweating.

The patient should be informed about these signs and instructed to notify the prescriber if they develop. Chronic overdosage is associated with accelerated bone loss and increased risk for atrial fibrillation, especially in older adults. Loss of bone increases the risk for fractures.

72
Q

What are the two major forms of hyperthyroidism?

A

There are two major forms of hyperthyroidism:Graves diseaseandtoxic nodular goiter(also known asPlummer disease).

73
Q

What are some s/s of hyperthyroidism?

A

nervousness, insomnia, rapid thought flow, and rapid speech. Skeletal muscles may weaken and atrophy. Metabolic rate is raised, resulting in increased heat production, increased body temperature, intolerance to heat, and skin that is warm and moist. Appetite is increased, weight loss

74
Q

Exophthalmos may develop, what is this?

A

the protrusion of one eye or both anteriorly out of the orbit.

75
Q

What causes hyperthyroidism?

A

Thyroid stimulation in Graves disease is caused by thyroid-stimulating immunoglobulins (TSIs), which are antibodies produced by an autoimmune process.

76
Q

What are the three treatment options for Graves disease?

A

(1) surgical removal of thyroid tissue
(2) destruction of thyroid tissue with radioactive iodine
(3) suppression of thyroid hormone synthesis with an antithyroid drug (methimazole or propylthiouracil).

77
Q

What would thyroid hormone levels look like in hyperthyroidism?

A

decreased TSH, increases T3 or T4

78
Q

What is a medication that may be used as adjunct therapy to treat certain symptoms?

A

β-Blockers and nonradioactive iodine may be used as adjunctive therapy. β-Blockers suppress tachycardia by blocking β-receptors on the heart. Nonradioactive iodine inhibits synthesis and release of thyroid hormones.

79
Q

What are s/s of thyroid storm?

A

Hyperthermia (105°F or even higher), severe tachycardia, restlessness, agitation, and tremor. Unconsciousness, coma, hypotension, and heart failure may ensue.

80
Q

What is the first-line drug for hyperthyroidism?

A

Methimazole (for Graves disease, adjunct to radiation therapy, to suppress thyroid hormone synthesis in preparation for thyroid gland surgery, it can be given to patients experiencing thyrotoxic crisis. Second PTU, third Radioactive iodine

81
Q

What is the MOA for methimazole?

A

Therapeutic effects result from blocking synthesis of thyroid hormones. Two mechanisms are involved. First, methimazole prevents the oxidation of iodide, thereby inhibiting incorporation of iodine into tyrosine. Second, methimazole prevents iodinated tyrosines from coupling. Both effects result from inhibiting peroxidase, the enzyme that catalyzes both reactions.

82
Q

What is the most dangerous adverse effect of Methimazole?

A

Agranulocytosis is the most dangerous toxicity.

83
Q

What monitoring is required for methimazole?

A

Methimazole can cause neonatal hypothyroidism, goiter, and even congenital hypothyroidism. Accordingly, the drug should be avoided during the first trimester. Use in the second and third trimesters is considered safe.

84
Q

What is the initial dose of Methimazole?

A

Initial: 30–40 mg, Maintenance: 5–15 mg

85
Q

How long should a patient be treated with Methimazole or PTU?

A

Treatment continues for 1–2 years

NR565 - Advanced Pharmacology (13 decks)

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