Exam 4: Endocrine Pharmacology Flashcards Preview

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Flashcards in Exam 4: Endocrine Pharmacology Deck (74):
1

Role of thyroid in infants:

Development of nervous system, growth

2

Thyroid gland secretes:

T3, T4, calcitonin

3

Thyroid hormones are made up of:

Two tyrosine molecules, iodinated, joined by ester linkage

4

More active form of thyroid hormone:

T3

5

Pathway to thyroid hormones:

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

6

Causes of hyperthyroidism:

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

7

Examples of thioamides/thioureylenes:

Propylthiouracil
Methimazole (Tapazole)

8

Indications for thioamides/thioureylenes:

Graves'
Hyperthyroidism
Only useful in overproduction situations

9

MoA of thioamides/thioureylenes:

Competes with thyroglobulin for iodide and reduces thyroid hormone synthesis

10

Onset of thioamides/thioureylenes:

1-2 weeks due to thyroid gland stores

11

A/E of thioamides/thioureylenes:

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

12

Preferred agent for hyperthyroidism and why:

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

13

Considerations for PTU:

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

14

A/E of PTU:

Depletes prothrombin so ↑ bleeding time

15

Additional hyperthyroid therapy beyond thioamides/thioureylenes:

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

16

β blockers for hyperthyroid:

Blocks peripheral conversion of T4 to T3, blocks adrenergic effects

17

Corticosteroids for hyperthyroid:

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

18

Iodide salts for hyperthyroid:

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

19

Causes of hypothyroidism:

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

20

PO synthroid:

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

21

A/E of synthroid:

Allergic rash

22

Indications for T3 vs. T4:

Myxedema coma

23

Drugs that increase levothyroxine metabolism:

Phenobarbital
Phenytoin
Rifampin
Carbamazepine

24

Drugs that decrease T4 to T3 conversion:

PTU
β blockers
Amiodarone
Glucocorticoids

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