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Pharmacology-Exam #1 (Summer) > Thyroid/Parathyroid > Flashcards

Thyroid/Parathyroid Flashcards

1
Q

Define thyroglobulin

A

Protein synthesized in the thyroid gland

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2
Q

Define Thyroxine-binding globulin (TBG)

A

Protein synthesized in the liver

Transports thyroid hormones in the blood

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3
Q

What is another name for TSH?

A

Thyrotropin

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4
Q

Lab findings in primary hypothyroidism

A 
Elevated TSH (>4.5 mIU/L)
Decreased serum free T4
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5
Q

Subclinical hypothyroidism lab values

A 
Elevated TSH (>4.5 mIU/L)
Normal serum free T4
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6
Q

When should Subclinical hypothyroidism be treated?

A

Iron deficiency anemia AND in patients with TSH >10

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7
Q

What is the most sensitive test for primary hypothyroidism and hyperthyroidism?

A

Serum TSH

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8
Q

Drugs that increase TSH

A
  1. Phenytoin
  2. Amiodarone
  3. Dopamine antagonist
  4. Excess estrogen or androgen
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9
Q

Disorders that may alter thyroid hormone lab values

A
  1. Pregnancy
  2. Chronic protein malnutrition
  3. Hepatic failure
  4. Nephrotic syndrome
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10
Q

What is the dose of a white tablet Levothyroxine

(Synthoid)?

A

50 mcg

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11
Q

What is the dosing of Levothyroxine? Half life?

A

Daily dosing

Half life= 7 days

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12
Q

When you change a dose of levothyroxine, when do you recheck a TSH and why?

A

Recheck TSH @ 6 weeks

Reaches steady state after 4-5 half lives

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13
Q

What can impair/reduce Levoythyroxine (T4) absorption?

A
  1. Food (take on empty stomach)
  2. H2 blockers and PPI’s
  3. Mucosal dz’s
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14
Q

Drugs that increase non-deiodinative T4 clearance

A
  1. Rifampin
  2. Carbamazepine
  3. Phenytoin
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15
Q

List the Synthetic T3 drug

A

Liothyronine

Cytomel

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16
Q

What is unique/disadvantage about Synthetic T3?

A

Rapid onset= Burst of energy
Short half life
Some is delivered too much to tissue than what is appropriate

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17
Q

List Synthetic T4:T3 (4:1) ratio drug

A

Liotrix

Throlar

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18
Q

Why does Synthetic T4:T3 LACK therapeutic rationale?

A

T4 is converted to T3 peripherally

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19
Q

What dose in the treatment of hypothyroidism do most patients require once they have reached steady state?

A

1.7 mcg/kg/day

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20
Q

What weight gives you a better estimate of a patient’s dose requirement?

A

Ideal Body Weight (IBW)

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21
Q

What it is the initial dose of Levothyroxine in young pt’s with long-standing dz and pt’s >45 WITHOUT known cardiac dz? When is it increased? Amount?

A

Initial dose= 50 mcg daily

Increased to 100 mcg after ONE month

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22
Q

What is the recommended initial daily dose for older patients OR those with known cardiac disease. When is is titrated up? Amount?

A

25 mcg per day

Titrated upward in increments of 25 mcg at monthly intervals

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23
Q

What percentage of pregnant women does the thyroxine dose requirement increase?Why?

A

75%

Fetus is very reliant on T4 during the 1st trimester

24
Q

What can excessive doses of thyroid hormone lead to?

A
  1. Heart failure
  2. Angina pectoris
  3. MI
25
Q

What levothyroxine tablet is the least allergenic?

A

0.05 mg (50 mcg)= White tablet

Dye FREE

26
Q

Result of hyperthyroidism in bones?

A

Hyperremodeling of cortical and trabecular bone= Reduced bone density=Increased risk of fx

27
Q

TSH-Suppressive Levothyroxine Therapy Indications

A
  1. Nodular thyroid dz and diffuse goiter: Suppress TSH to low-normal levels (0.5-1)
  2. Hx of thyroid irradiation
  3. Thyroid CA: Higher risk pt’s (TSH <0.1), Lower-risk pt’s (0.1-0.5)
28
Q

What drugs can hypothyroidism effect the distribution?

A
  1. Digoxin-Higher serum values

2. Warfarin: Decreases sensitivity d/t lower metabolism of Vitamin K

29
Q

What are the cardinal si/sx’s in HYPERthyroidism?

A
  1. Weight loss

2. Increased appetite

30
Q

What si/sx’s are specific to Grave’s disease (Hypothyroidism)?

A
  1. Exopthalmos

2. Pretibial Myxedema

31
Q

What is first-line hyperthyroidism treatment in children, adolescents, and in pregnancy?

A

Antithyroid drugs:

  • Propothyrouracil (PTU)
  • Methimazole (MMI)*
32
Q

Propothyrouracil (PTU) and Methimazole (MMI) MOA

A

Inhibit coupling of monoiodotyrosine and diiodotyrosine to form T4 and T3

33
Q

How many weeks does it take for sx’s to diminish and circulating thyroid hormone levels return to normal?

A

4-8 weeks

34
Q

When should changes in PTU and MMI doses for each drug be made?

A

Monthly

35
Q

What is the MC ADE of PTU and MMI?

A

Hepatoxicity

36
Q

Other PTU and MMI. ADE’s?

A
  1. Rash
  2. Leukopenia (benign)
  3. Agranulocytosis
  4. Arthralgias and a lupus-like syndrome
37
Q

When is the ONLY time that PTU is considered a first-line drug treatment? Why?

A

Frist Trimester of pregnancy

MMI teratogenic effects outweighs that of PTU-associated hepatoxicity

38
Q

When should Potassium iodide be administered?

A

7-14 days preoperatively (general surgery)

39
Q

As an adjunct to radioactive iodine, when should saturated solution potassium iodide (SSKI) be administered? Why?

A

3-7 days AFTER RAI treatment

Allow that radioactive iodide to concentrate in the thyroid

40
Q

Iodide ADE’s

A
  1. Salivary gland swelling

2. “Iodism”: Metallic taste, burning mouth/sore throat,, sore teeth/gums; gynecomastia

41
Q

What can you prescribe for symptom relief in hyperthyroidism?

A

Propranolol

42
Q

What is the advantage of radioactive iodine? When is this the best treatment option?

A

Hyperthyroidism cure

Best treatment for toxic nodules and toxic multinodular goiter

43
Q

What are the disadvantage of radioactive iodine?

A
  1. Permanent hypothyroidism almost inevitable

2. Pregnancy must be deferred for 6–12 months; no breast-feeding

44
Q

When is surgery for hyperthyroidism the best option?

A
  • In pregnancy if major S/E from antithyroid drugs

- Coexisting suspicious nodule present

45
Q

Lab findings in hypoparathyroidism

A

HYPOcalcemia
HYPERphosphatemia
HYPERcalciruia

46
Q

What is crucial for PTH secretion and activation of the PTH receptor?

A

Magnesium

47
Q

hypoparathyroidism treatment

A
  1. Oral calcium carbonate
  2. Calcitrol (Vitamin D 1,25)
  3. Phosphate binders: If high calcium-phosphate
48
Q

Define primary hyperparathyroidism

A

Intrinsic parathyroid gland dysfunction resulting in excessive secretions of PTH with a lack of response to feedback inhibition by elevated calcium

49
Q

Define secondary hyperparathyroidism

A

Excessive secretion of PTH in response to hypocalcemia

50
Q

Causes for secondary hyperparathyroidism?

A
  1. Vitamin D deficiency

2. Renal failure

51
Q

What PTH level suggest primary hyperparathyroidism?

A

High PTH (>3.0 pmol/L)

52
Q

What PTH level suggest non-PTH-mediated hypercalcemia?

A

Low PTH (<3.0 pmol/L)

53
Q

What is the curative treatment for primary hyperparathyroidism?

A

Surgery

54
Q

Secondary hyperparathyroidism treatment

A
  1. Calcium replacement
  2. Vitamin D analogues: paricalcitol and calcitriol
  3. Phosphorus-binding agents: sevelamer
  4. Calcimimetic: cinacalcet)
55
Q

What are the advantages of Antithyroid drugs?

A
  1. Noninvasive*

2. Low risk of permanent hypothyroidism

56
Q

What are the disadvantages of Antithyroid drugs?

A

Low cure rate (Avg=40-50%)

Pharmacology-Exam #1 (Summer) (6 decks)

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