Exam 4: Endocrine Pharmacology Flashcards

(74 cards)

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
Drugs that decrease absorption of levothyroxine from the gut:
``` Cholestyramine FeSO4 Aluminum hydroxide Sucralfate Kayexalate ```
26
Drugs that ↑ thyroid binding globulin and bind T4/T3:
Pregnancy | Estrogen
27
Amiodarone and thyroid status:
Structurally resembles TH, can make hypo or hyperthyroid
28
Lithium and thyroid status:
Actively concentrates in thyroid gland and can inhibit TH synthesis → hypothyroid
29
Reglan and thyroid status:
↑ TSH production/release
30
Natural forms of corticosteroids:
Cortisol, cortisone, aldosterone
31
Synthetic forms of corticosteroids:
Prednisolone, prednisone, methylprednisone, dexamethasone
32
Mineralocorticoid effects:
AKA aldosterone | Reabsorption of Na+ and excretion of K+ in distal tubule
33
Glucocorticoid effects:
AKA cortisol Antiinflammatory Augmentation of sustained SNS activity during periods of emotional or physical stress
34
MoA of corticosteroids:
Enter cells, bind to steroid receptors in cytoplasm, enter nucleus, influence protein synthesis (mostly metabolic/inflammatory)
35
Mineralocorticoid receptors found:
Organs of excretion | Colon, glands, kidney, hippocampus
36
Glucocorticoid receptors found:
Everywhere
37
Metabolic effects of corticosteroids:
↑ BG, amino acids, TGs
38
Inflammation effects of corticosteroids:
Inhibition of phospholipase A2 → decreased arachidonic acid formation
39
Endogenous cortisol secretion:
By circadian pattern Avg 10-20 mg/day 50-150 mg/day under extreme stress
40
PK of cortisol:
90% protein bound 70% metabolized in liver E1/2t: 1.5 - 3 hrs
41
Methylprednisolone highlights:
Intensely glucocorticoid, IV/intraarticular, used as replacement for insufficiency
42
Betamethasone highlights:
PO/IV; lacks mineralocorticoid effects
43
Dexamethasone highlights:
PO/IV; good for cerebral edema, antiemesis, airway edema
44
Triamcinolone highlights:
PO, IV, intraarticular; LBP epidural injections
45
Prednisolone highlights:
PO/IV; mineralocorticoid and glucocorticoid effects
46
Indications for corticosteroids:
``` Replacement tx Antiinflammatory Adrenal insufficiency Allergy/asthma Antiemetic ```
47
Chronic adrenal insufficiency dosing:
Cortisone PO 25mg Q AM 12.5 MG Q PM Usually add fludrocortisone
48
Acute adrenal insufficiency dosing:
Cortisol | 100mg Q8hr
49
Timeline for corticosteroid effects in acute allergy/asthma:
1 hr to β-agonist enhancement (aka makes epi work better) | 4-6 hrs to antiinflammatory effects
50
Considerations for chronic allergy/asthma management with corticosteroids:
80-90% MDI dose swallowed, can lead to dysphonia | Generally no HPA axis problems until daily doses > 1500mcg adult/400mcg peds
51
Best corticosteroid to use as antiemetic:
Dexamethasone 8-10mg IV; E1/2t is 3 hrs, antiemetic effect lasts up to 24
52
Corticosteroids for lumbar disc herniation:
Triamcinolone 25-50mg or methylprednisolone 40-80mg for epidural injection HPA axis suppression for 1-3 months
53
Intra-op sequelae of HPA axis suppression:
CV collapse
54
Synthesis of glucagon:
Produced by α cells of pancreas in response to hypoglycemia or ↑ plasma proteins
55
MoA of glucagon:
NON-ADRENERGIC enhancement of cAMP formation
56
Effects of glucagon:
``` ↑ myocardial contractility/HR ↑ renal blood flow ↑ insulin secretion ↑ gluconeogenesis/glycogenolysis ↑ catecholamine release ``` ↓ gastric motility Relaxation of smooth muscle/vasodilator
57
Indications for glucagon:
``` ↑ 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
Dosage of glucagon:
1-5mg IV or 5mcg/kg/min
59
A/E of glucagon:
Hyperglycemia (or paradoxical hypoglycemia) Hypokalemia N/V Abrupt ↑ in HR in afib
60
MoA of octreotide/somatostatin:
Inhibit hormone release from GI tract/pancreas (GH, insulin, glucagon, VIP)
61
Indications for octreotide/somatostatin:
Carcinoid crisis Hepatorenal syndrome Esophageal varices
62
Half-time of somatostatin vs. octreotide:
Somatostatin: 3 min Octreotide: 2.5 hours
63
ADH action at V2:
Collecting ducts in nephron - ↑ water permeability back into circulation
64
ADH action at V1:
Arterial smooth muscle vasoconstriction (takes large doses)
65
Half-time of vasopressin:
10-20 min
66
Indications for vasopressin:
DI Esophageal varices (gets blood out of splanchnic circ) Hemorrhagic/septic shock ACLS
67
A/E of vasopressin:
↑ BP Coronary vasoconstriction GI hyperperistalsis
68
DDAVP vs. vasopressin:
DDAVP = vasopressin analogue with longer half-time (2.5 - 4.4 hrs), more selective for V2 vs. V1, better choice for DI
69
DDAVP effects on endothelial cells:
Stimulates secretion of vWF, tissue plasminogen activator, prostaglandins
70
Labor induction dose of oxytocin:
1-2 mU/min, increase 15-30 min by 1-2 mU/min until contractions 2-3 min apart
71
Uterine atony dose of oxytocin:
Up to 40 mU/min
72
Anesthetic consideration for oxytocin:
Blunted compensatory responses can see hypotension with oxytocin
73
MoA of estrogen and progesterone:
Estrogen: prevents FSH release Progesterone: prevents LH release
74
A/E of ovarian hormones:
Thromboembolism MI/stroke risk HTN risk