Pharm 38 Objectives Flashcards

1
Q

What are the 3 main steroid products of the adrenals.

A
  • Glucocorticoid
  • Mineralocorticoid
  • Androgens
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2
Q

What is the primary physiologic glucocorticoid?

A

Cortisol

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3
Q

What is the primary pharmacologic congener of glucocorticoid?

A

Hydrocortisone

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4
Q

What is the primary physiologic mineralocorticoid?

A

Aldosterone

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5
Q

What is the primary pharmacologic congener of mineralocorticoid?

A

Fludrocortisone

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6
Q

What is the primary drug therapy option for Addison’ and its typical dosing regimen?

A
  • Hydrocortisone

- Dose: 2/3 in am and 1/3 in afternoon

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7
Q

What medication is used as an adjunct drug therapy to support blood pressure, if needed?

A

Fludrocortisone (potent mineralocorticoid)

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8
Q

When is the most appropriate time(s) of day to dose the glucocorticoid (and mineralocorticoid if necessary)?

A

Give most of the dose in the AM and smaller doses throughout the day
- 2/3 in AM and 1/3 in afternoon

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9
Q

When should you dose adjustment glucocorticoid (and mineralocorticoid if necessary)?

A
  • Dosage is increase in times of stress —> double the dose

- If surgery dose may need to be greatly increased for 48-72 hrs

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10
Q

What is T3?

A

Active thyroid hormone

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11
Q

What is the Physiologic Abundance of T3?

A
  • 20% secreted by thyroid gland

- Most produced from T4 in the liver

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12
Q

What is the Biologic activity of T3?

A

Activates gene transcription leading to increase syntheses of proteins necessary for growth development, and calorigenesis (heat production)

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13
Q

What is the onset of T3?

A

Within a few hours

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14
Q

What is the duration/half life of T3?

A

Approx. 1 day

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15
Q

What is T4?

A
  • Inactive thyroid hormone

- Precursor for T3

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16
Q

What is the Physiologic Abundance of T4?

A
  • 80% secreted by thyroid gland.

- Produced in thyroid gland and stored in thyroid follicles

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17
Q

What is the Biologic activity of T4?

A

Some of T4 is converted to T3 in liver and muscles and this conversion is the final step of thyroid activity
- T4 can also be converted into reverse T3 (rT3) which is the inactive and stored form of the hormone—> this is seen in pts taking too much T4

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18
Q

What is the onset of T4?

A

3-5 days

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19
Q

What is the duration/half life of T4?

A

Approx. 7 days

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20
Q

What pharmacologic product contains T4? and “who is best pt” for this drug?

A

Levothyroxine (T4)

  • Can be used on its own
  • Preferred thyroid supplement for most pts
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21
Q

What pharmacologic product contains T3? and “who is best pt” for this drug?

A

Liothyronine (T3)

- Used in pts who doesn’t get adequate convert T4 to T3.

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22
Q

What are CI with Liothyronine (T3)?

A
  • Should not be used on it own for thyroid supplement

- Do not use in pts with cardiac issues

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23
Q

What pharmacologic product contains T4 and T3? and what can it cause?

A

“Thyroid USP” or Desiccated Porcine Thyroid Extract (T4 and T3)

  • Animal based: ground up pig thyroid “natural product”
  • Can cause over stimulation of the heart and thyroid
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24
Q

What are the 2 Thyroid synthesis inhibitors used in Hyperthyroidism?

A
  • Propylthiouracil (PTU)

- Methimazole

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25
Q

What is the duration/half life and how long does it take to reach Euthyroid state with Propylthiouracil (PTU)?

A
  • Short half-life, required TID

- 6-12 mos for euthyroid state

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26
Q

What are the ASEs of Propylthiouracil (PTU)?

A
  • Agranulocytosis
  • Not always able to establish a euthyroid state: may lead to hypothyroidism
  • Concerns w/ pregnancy and lactation
  • Severe liver damage
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27
Q

What is the duration/half life and how long does it take to reach Euthyroid state with Methimazole?

A
  • Longer half live, once-daily dosing

- May take 3-12 wks for euthyroid state

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28
Q

Methimazole is an adjunct therapy to what?

A

Thyroid irradiation

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29
Q

What are the ASEs of Methimazole

A
  • Agranulocytosis

- MORE dangerous than PTU during lactation and during the 1st trimester of pregnancy

30
Q

What is the role of Beta Blockers for pts with hyperthyroidism?

A
  • Use for occasional or short time only for symptomatic tx not tx hyperthyroidism
  • Longer term use can cause problems during pregnancy
31
Q

What Beta Blocker is most commonly used in pts with hyperthyroidism?

A

Non selective: Propranolol

- Suppress: tachy, tremors, anxiety, and others

32
Q

Why is it important to screen for and closely monitor hypothyroidism during pregnancy?

A
  • During 1st trimester insufficient thyroid hormones can result in permanent neuropsychologic deficits in child.
33
Q

How is thyroid dosing adjusted during pregnancy?

A

Frequently increasing during pregnancy

34
Q

Why is Hypothyroidism in infants a concern?

A
  • May be permanent or transient

- Can cause mental retardation and derangement of growth

35
Q

What are the concerns with use of thyroid synthesis inhibitors for Hyperthyroidism during pregnancy?

A
  • Only use or moderate to severe hyperthyroidism

- PTU and Methimazole readily cross the placenta and both are FDA cat. D

36
Q

What are the BBW for Methimazole and PTU?

A
  • D/t fetal abnormalities associated with Methimazole, PTU may be the tx of choice when antithyroid an drug is indicated during or just prior during the 1st trimester
  • Liver tox is higher with PTU the use of Methimazole may be preferred during the 2nd or 3rd trimester
37
Q

How often should maternal thyroid fxn be monitored?

A

Monitored after 2wks of TSI has been initiated and then every 2 to 4 wks.

38
Q

PTU is a treatment for what thyroid emergency in pregnant women?

A

Thyroid Storm

39
Q

What medication is the most notorious for causing thyroid disorders? and why?

A

Amiodarone

  • Increases risk for thyroid disease in 1 year by 10x
  • Can cause both Hyperthyroidism and Hypothyroidism
40
Q

What are some other medications the can cause thyroid disorders?

A
  • Tyrosine Kinase inhibitors (chemo drugs)
  • Lithium
  • Interleukin-2
  • Interferon-alfa
41
Q

What is the secretory product of Pancreatic a-cells?

A

Glucagon

42
Q

What is the secretory product of Pancreatic b-cells?

A

Insulin and amylin

43
Q

What is the secretory product of Pancreatic δ-cells?

A

Somatostatin

44
Q

What is the secretory product of Pancreatic g-cells?

A

Gastrin

45
Q

What is the secretory product of Pancreatic f-cells?

A

Pancreatic polypeptide

46
Q

What is the role of intestinal L-cells?

A

Synthesize proglucagon which is converted to glucagon-like peptide “GLP”

47
Q

What is the pharmacological product of Pancreatic a-cells?

A

Glucagon for injection

48
Q

What is the pharmacological product of Pancreatic b-cells?

A

Many insulin products (ie amylin —> pramlintide)

49
Q

What is the pharmacological product of Pancreatic δ-cells?

A

Octreotide

50
Q

What does Somatostatin inhibit?

A

Somatostatin causes widespread inhibition of endocrine and exocrine fx of pancreas, gall bladder, and gut

51
Q

What does Somatostatin regulate?

A

Secretion of alpha and beta pancreatic cells

52
Q

What are the indications of Octreotide?

A
  • Acromegaly
  • Metastatic, carcinoid tumors
  • Vasoactive intestinal peptide-secreting tumor
53
Q

What is the 1st step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. Increased blood glucose -GLUT2-> increased intracellular glucose
54
Q

What is the 2nd step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. The metabolism of glucose causes a rise in the ATP:ADP ratio
55
Q

What is the 3rd step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. Increase ATP/ADP inactivated K+ channel
56
Q

What is the 4th step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. Depolarization of the membrane
57
Q

What is the 5th step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. Ca2+ channel opens
58
Q

What is the 6th step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. Intracellular Ca2+ levels increase
59
Q

What is the 7th step of the 7 steps in insulin secretion and how the beta-cell acts as a glucose sensor?

A
  1. Exocytotic release of insulin from storage granules
60
Q

What cells produce Glucagon?

A

Alpha cells of the pancreases in response to decreased blood glucose concentration

61
Q

How does glucagon act as a counter-regulatory concentration?

A
  • When blood sugar levels are high, glucose enters the alpha cells and is converted to ATP
  • When ATP levels are high, ATP- gated potassium channels remain open
  • When BG falls, ATP levels in the cell fall, with low ATP the ATP gated potassium channels close.
62
Q

When fasting is insulin still be secreted?

A

Even when fasting, insulin is secreted around the clock but at low rate which results in low plasma insulin concentration.

63
Q

How does basal and prandial vary based on physiologic serum insulin levels?

A
  • If BG suddenly rises insulin is quickly secreted and rises to 10x the basal level within 3-5 minutes
  • Insulin levels decrease after about 10 minutes but if glucose levels cont. to be elevated for much longer then insulin concentrations increase even higher than initial rise
64
Q

How does b-cell secretagogue drugs stimulate the release of insulin?

A

Increase the release of insulin from pancreatic beta cells by:

  • Inhibiting ATP sensitive potassium channels in the plasma membrane
  • Decrease glucagon secretion
65
Q

What are the physiologic effect of insulin?

A

Anabolic hormone:

  • cell growth, differentiation, gene expression
  • “storage hormone”, increases synthesis of glycogen, lipids, carbs and protein while inhibiting their breakdown
  • Insulin reduces glucose output by the liver
66
Q

Insulin activates what transporter? and what does the activation result in?

A
  • GLUT4

- Promotes uptake of glucose by skeletal muscles and adipose tissue

67
Q

What is Insulin used for in a medical setting? and what do we measure?

A
  • Treat DM

- Measure the effects of insulin to increase cellular uptake of glucose

68
Q

An increased expression of glucose transport proteins allows for what?

A

Cellular use of glucose for energy

69
Q

What is seen when a DM pt is treated with insulin?

A

Decrease in blood/plasma glucose concentration

70
Q

What are the 2 indications for the laboratory assessment of hemoglobin glycosylation A1c?

A
  • Diagnosis of DM

- Glycemic goals for DM pts

71
Q

What are glycemic goals for DM pt decided?

A
  • Clinicians + patients determine a specific A1c goal for each pt.
  • Want a realistic goal: don’t want pt to drop to hypoglycemia
72
Q

What does the A1c measure and how often should it be rechecked?

A
  • Approximated average of glycemia over the previous 3 mos

- Should be re-checked every 3 mos