Exam 4: Endocrine Pharmacology Flashcards

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1
Q

Role of thyroid in infants:

A

Development of nervous system, growth

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2
Q

Thyroid gland secretes:

A

T3, T4, calcitonin

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3
Q

Thyroid hormones are made up of:

A

Two tyrosine molecules, iodinated, joined by ester linkage

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4
Q

More active form of thyroid hormone:

A

T3

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5
Q

Pathway to thyroid hormones:

A

Hypothalamus releases TRH → anterior pituitary releases TSH → thyroid secretes T4 > T3 → conversion in periphery

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6
Q

Causes of hyperthyroidism:

A

Graves’: IgG antibody activates TSH receptor
Toxic multinodular goiter
Iatrogenic (overdose)
Pit tumor, thyroid cancer, testicular cancer (βhCG release)

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7
Q

Examples of thioamides/thioureylenes:

A

Propylthiouracil

Methimazole (Tapazole)

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8
Q

Indications for thioamides/thioureylenes:

A

Graves’
Hyperthyroidism
Only useful in overproduction situations

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9
Q

MoA of thioamides/thioureylenes:

A

Competes with thyroglobulin for iodide and reduces thyroid hormone synthesis

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10
Q

Onset of thioamides/thioureylenes:

A

1-2 weeks due to thyroid gland stores

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11
Q

A/E of thioamides/thioureylenes:

A
Goiter d/t ↑ TSH stimulating thyroid hypertrophy
Pruritic rash
Arthralgias
Agranulocytosis
Hepatotoxicity
Vasculitis/drug-induced lupus
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12
Q

Preferred agent for hyperthyroidism and why:

A

Methimazole d/t longer half-life, once daily dosing, more potent, less serious A/E

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13
Q

Considerations for PTU:

A

Inhibits conversion of T4 to T3 in periphery
TID dosing
Preferred in pregnancy and thyroid storm
No IV formulation

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14
Q

A/E of PTU:

A

Depletes prothrombin so ↑ bleeding time

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15
Q

Additional hyperthyroid therapy beyond thioamides/thioureylenes:

A
I131
Surgical resection
β blockers
Corticosteroids
Iodide salts (Lugol's)
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16
Q

β blockers for hyperthyroid:

A

Blocks peripheral conversion of T4 to T3, blocks adrenergic effects

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17
Q

Corticosteroids for hyperthyroid:

A

Blocks peripheral conversion of T4 to T3, suppresses antibodies and inflammation

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18
Q

Iodide salts for hyperthyroid:

A

Blocks peripheral conversion of T4 to T3, decreases vascularity of thyroid gland, temporarily blocks TH release due to gland being occupied with iodide uptake

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19
Q

Causes of hypothyroidism:

A

Hashimoto’s: antibodies against thyroid gland proteins
Thyroid ablation/surgery
Iodine-containing drugs
Pit tumor

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20
Q

PO synthroid:

A

Synthesized T4
Long half-life (7 days)
Monitor TSH, T4

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21
Q

A/E of synthroid:

A

Allergic rash

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22
Q

Indications for T3 vs. T4:

A

Myxedema coma

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23
Q

Drugs that increase levothyroxine metabolism:

A

Phenobarbital
Phenytoin
Rifampin
Carbamazepine

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24
Q

Drugs that decrease T4 to T3 conversion:

A

PTU
β blockers
Amiodarone
Glucocorticoids

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25
Q

Drugs that decrease absorption of levothyroxine from the gut:

A
Cholestyramine
FeSO4
Aluminum hydroxide
Sucralfate
Kayexalate
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26
Q

Drugs that ↑ thyroid binding globulin and bind T4/T3:

A

Pregnancy

Estrogen

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27
Q

Amiodarone and thyroid status:

A

Structurally resembles TH, can make hypo or hyperthyroid

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28
Q

Lithium and thyroid status:

A

Actively concentrates in thyroid gland and can inhibit TH synthesis → hypothyroid

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29
Q

Reglan and thyroid status:

A

↑ TSH production/release

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30
Q

Natural forms of corticosteroids:

A

Cortisol, cortisone, aldosterone

31
Q

Synthetic forms of corticosteroids:

A

Prednisolone, prednisone, methylprednisone, dexamethasone

32
Q

Mineralocorticoid effects:

A

AKA aldosterone

Reabsorption of Na+ and excretion of K+ in distal tubule

33
Q

Glucocorticoid effects:

A

AKA cortisol
Antiinflammatory
Augmentation of sustained SNS activity during periods of emotional or physical stress

34
Q

MoA of corticosteroids:

A

Enter cells, bind to steroid receptors in cytoplasm, enter nucleus, influence protein synthesis (mostly metabolic/inflammatory)

35
Q

Mineralocorticoid receptors found:

A

Organs of excretion

Colon, glands, kidney, hippocampus

36
Q

Glucocorticoid receptors found:

A

Everywhere

37
Q

Metabolic effects of corticosteroids:

A

↑ BG, amino acids, TGs

38
Q

Inflammation effects of corticosteroids:

A

Inhibition of phospholipase A2 → decreased arachidonic acid formation

39
Q

Endogenous cortisol secretion:

A

By circadian pattern
Avg 10-20 mg/day
50-150 mg/day under extreme stress

40
Q

PK of cortisol:

A

90% protein bound
70% metabolized in liver
E1/2t: 1.5 - 3 hrs

41
Q

Methylprednisolone highlights:

A

Intensely glucocorticoid, IV/intraarticular, used as replacement for insufficiency

42
Q

Betamethasone highlights:

A

PO/IV; lacks mineralocorticoid effects

43
Q

Dexamethasone highlights:

A

PO/IV; good for cerebral edema, antiemesis, airway edema

44
Q

Triamcinolone highlights:

A

PO, IV, intraarticular; LBP epidural injections

45
Q

Prednisolone highlights:

A

PO/IV; mineralocorticoid and glucocorticoid effects

46
Q

Indications for corticosteroids:

A
Replacement tx
Antiinflammatory
Adrenal insufficiency
Allergy/asthma
Antiemetic
47
Q

Chronic adrenal insufficiency dosing:

A

Cortisone PO
25mg Q AM
12.5 MG Q PM
Usually add fludrocortisone

48
Q

Acute adrenal insufficiency dosing:

A

Cortisol

100mg Q8hr

49
Q

Timeline for corticosteroid effects in acute allergy/asthma:

A

1 hr to β-agonist enhancement (aka makes epi work better)

4-6 hrs to antiinflammatory effects

50
Q

Considerations for chronic allergy/asthma management with corticosteroids:

A

80-90% MDI dose swallowed, can lead to dysphonia

Generally no HPA axis problems until daily doses > 1500mcg adult/400mcg peds

51
Q

Best corticosteroid to use as antiemetic:

A

Dexamethasone 8-10mg IV; E1/2t is 3 hrs, antiemetic effect lasts up to 24

52
Q

Corticosteroids for lumbar disc herniation:

A

Triamcinolone 25-50mg or methylprednisolone 40-80mg for epidural injection
HPA axis suppression for 1-3 months

53
Q

Intra-op sequelae of HPA axis suppression:

A

CV collapse

54
Q

Synthesis of glucagon:

A

Produced by α cells of pancreas in response to hypoglycemia or ↑ plasma proteins

55
Q

MoA of glucagon:

A

NON-ADRENERGIC enhancement of cAMP formation

56
Q

Effects of glucagon:

A
↑ myocardial contractility/HR
↑ renal blood flow
↑ insulin secretion
↑ gluconeogenesis/glycogenolysis
↑ catecholamine release

↓ gastric motility
Relaxation of smooth muscle/vasodilator

57
Q

Indications for glucagon:

A
↑ CO in β overblockade
Biliary dilation
Improves low CO, CHF
Enhanced AV node conduction in dig toxicity
Dx of pheo

Really only good for acute situations

58
Q

Dosage of glucagon:

A

1-5mg IV or 5mcg/kg/min

59
Q

A/E of glucagon:

A

Hyperglycemia (or paradoxical hypoglycemia)
Hypokalemia
N/V
Abrupt ↑ in HR in afib

60
Q

MoA of octreotide/somatostatin:

A

Inhibit hormone release from GI tract/pancreas (GH, insulin, glucagon, VIP)

61
Q

Indications for octreotide/somatostatin:

A

Carcinoid crisis
Hepatorenal syndrome
Esophageal varices

62
Q

Half-time of somatostatin vs. octreotide:

A

Somatostatin: 3 min
Octreotide: 2.5 hours

63
Q

ADH action at V2:

A

Collecting ducts in nephron - ↑ water permeability back into circulation

64
Q

ADH action at V1:

A

Arterial smooth muscle vasoconstriction (takes large doses)

65
Q

Half-time of vasopressin:

A

10-20 min

66
Q

Indications for vasopressin:

A

DI
Esophageal varices (gets blood out of splanchnic circ)
Hemorrhagic/septic shock
ACLS

67
Q

A/E of vasopressin:

A

↑ BP
Coronary vasoconstriction
GI hyperperistalsis

68
Q

DDAVP vs. vasopressin:

A

DDAVP = vasopressin analogue with longer half-time (2.5 - 4.4 hrs), more selective for V2 vs. V1, better choice for DI

69
Q

DDAVP effects on endothelial cells:

A

Stimulates secretion of vWF, tissue plasminogen activator, prostaglandins

70
Q

Labor induction dose of oxytocin:

A

1-2 mU/min, increase 15-30 min by 1-2 mU/min until contractions 2-3 min apart

71
Q

Uterine atony dose of oxytocin:

A

Up to 40 mU/min

72
Q

Anesthetic consideration for oxytocin:

A

Blunted compensatory responses can see hypotension with oxytocin

73
Q

MoA of estrogen and progesterone:

A

Estrogen: prevents FSH release
Progesterone: prevents LH release

74
Q

A/E of ovarian hormones:

A

Thromboembolism
MI/stroke risk
HTN risk