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Endocrine - Matt > SM159 Pharm > Flashcards

SM159 Pharm Flashcards

1
Q

Desmopressin

A

ADH analog, long-acting

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2
Q

Vasopressin mechanism

A

Acts through GPCR
V1 receptors: couples to PLC, releases Ca++, causes vasoconstriction and CNS effects
V2 receptors: couples to AC to increase cAMP, increases water reabsorption in the collecting duct via insertion and stabilization of aquaporins, increases factor VIII and vWF

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3
Q

Is desmopressin or vasopressin more potent? Which as a longer half-life?

A

Desmo has a 4000x greater antidiurietic/pressor activity

Desmo also has a longer half-life

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4
Q

Vasopressin pharmacokinetics

A

Hepatic/renal metabolism

Reduction of disulfide bond

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5
Q

Vasopressin indications

A 
Central DI (inadequate release of vasopressin)
Stop esophageal varices bleeding
Stop bleeding in hemophilia A and vW disease
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6
Q

Vasopressin adverse effects

A 
Undesired vasoconstriction (like in patients with CAD)
Nausea, cramps, headaches, allergic rxn
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7
Q

Nephrogenic DI: etiology, treatment

A

Impaired renal response to ADH

Treat with thiazides

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8
Q

SIADH: etiology, treatment

A

Malignancy, head injury, drugs

Conivaptan, tolvaptan: vasopression receptor antagonists

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9
Q

Oxytocin mechanism

A

Binds GPCR, releases Ca++ via PLC. Also causes release of prostaglandins and leukotrienes.

Actions: leads to smooth muscle contraction, stimulates uterine contraction, causes milk ejection.

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10
Q

Oxytocin indications

A

Induce labor when early vaginal delivery is indicated (eclampsia) or when labor is protracted or arrested

Postpartum to control uterine hemorrhage

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11
Q

Oxytocin adverse effects

A

Uterine rupture, fetal distress, activation of vasopressin receptors

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12
Q

GH analogs

A

Somatropin: identical
Somatrem: + methionine (extends half life)

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13
Q

GH regulation

A

Stimulated by GHRH

Inhibited by SS and dopamine

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14
Q

GH mechanism

A

Acts through TYK receptors, activates JAKs which activate STAT proteins. Stimulate release of IGF-1.

Actions: stimulates longitudinal growth of bone before plates close, increase muscle mass, decrease central fat, reduce sensitivity to insulin, increase glycolysis

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15
Q

GH indications

A

Replacement therapy for GH deficient kids
Other causes of short stature: Turner, Prader-Willi, chronic renal insufficiency
AIDS wasting
Abuse: antiaging, athletic enhancement

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16
Q

GH adverse effects

A

Joint and muscle pain, peripheral edema, carpal tunnel, insulin resistance, adrenal insufficiency due to inhibition of 11b-hydroxysteroid dehydrogenase

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17
Q

IGF-1 agonists

A

Sometimes GH response is inadequate, so use these

Mecasermin: recombinant form
Mecasermin rinfabate: contains IGF-1 and IGF-1 binding protein (IGFBP-3) that extends the half-life and stimulates uptake into cells

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18
Q

Mecasermin indications

A

Promote growth and normalize metabolism in cases of GH deficiency that are resistant to GH

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19
Q

Mecasermin adverse effects

A

Hypoglycemia, lipohypertrophy, slipped epiphyses, scoliosis

Contraindicated in people with cancer

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20
Q

Somatostatin analog

A

Octreotide

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21
Q

Somatostatin analogs indications

A

Acromegaly: abnormal growth of bone and cartilage

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22
Q

Octreotide adverse effects

A

Nausea and bloating, gall stones, bradycardia

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23
Q

Octreotide mechanism

A

Acts through SS receptors (GPCR), activates K+ channels and protein phosphotyrosine phosphotases

Actions: inhibits GH secretion, inhibits secretion of TSH, ACTH, glucagon, gastrin, and insulin

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24
Q

Pegvisomant mechanism

A

Allows receptor dimerization but blocks signaling in the JAK-STAT pathway

25
Q

Pegvisomant adverse effects

A

Increase in liver transaminases, lipohypertrophy, compulsive behavior, GH-secreting adenomas

26
Q

Bromocriptine and cabergoline mechanism

A

Selective dopamine D2 agonists, mimic effects of dopamine to inhibit GH production and secretion

Also inhibit prolactin

27
Q

Bromocriptine and cabergoline adverse effects

A

Nausea, vomiting, headache, orthostatic hypotension

28
Q

Generic names for thyroid hormones, other preparation used

A 
T4 = levothyroxine
T3 = liothyronine
Liotrix = T4/T3 combination
29
Q

Thyroid hormones mechanisms

A

Act as heterodimers through nuclear receptors to regulate genes. Receptors with no ligand bound acts as repressors.

4 major types: a1, a2, b1, b2

30
Q

Thyroid hormone tissue differences

A

b1 > a1 in liver
b2 in hypothalamus
a2 is a non-binding inactive form

31
Q

Thyroid hormones role in development

A

Critical for CNS development (inadequacy gives you cretinism) both during gestation and postpartum

Critical for skeleton development

32
Q

Thyroid hormones non-development effects

A

Metabolic: important for optimal energy metabolism and reproductive function

Cardiac: inotropic and chronotropic effects; potentiate effects of sympathomimetic amines

Hepatic: increase cholesterol metabolism; effects on glucose metabolism cause insulin resistance

Skeletal: excess thyroid hormone can promote osteoporosis, especially in adults

33
Q

Target genes for thyroid hormones

A 
Myelin basic protein
Ca++ ATPase in skeletal muscle
Ion channel protein in pacemaker
b-adrenergic receptors
IGF-1
34
Q

T4 to T3 conversion

A

5’-deiodination in the periphery (blocked by beta-blockers)

35
Q

T3 or T4: which is more potent, better cleared, binds less proteins, and cleared faster? Which one is most commonly used and why?

A

T3 is better in each category

T4 is more commonly used: more convenient dosage and lower risk

36
Q

Thyroid hormone indications

A

Hypothyroidism: Hashimoto’s, destruction by medical treatment, secondary

37
Q

Thyroid hormone adverse effects

A

Weight loss, sweating, diarrhea, anxiety, headaches

Palpitations, angina, thrombosis (due to beta-adrenergic signaling)

Chronic: weakness, anemia, infertility, HF, bone loss, insulin resistance

38
Q

T3/T4 production mechanism

A

Iodide is transported into the follicular cells, peroxidase oxidizes iodide and couples it to thyroglobulin to produce MIT and DIT (target of antithyroid drugs), two DIT get put together and then proteolysis gives you T4

T4 is turned into T3 in the periphery

39
Q

Radioactive iodide (131 I) mechanism

A

Gamma and beta emitter
131 I gets trapped, incorporated, and deposited into the colloid
Released beta particles cause necrosis of follicular cells without damaging nearby cells

40
Q

Methimazole and propylthioruacil mechanism

A

Thionamides: used for hyperthyroidism

Inhibit thyroid peroxidase (PTU also blocks T4 to T3 conversion in the periphery)

41
Q

Thionamide adverse effects

A

Pruritic rash, arthralgia
Agranulocytosis is rare but fatal
Give PTU in pregnancy

42
Q

Role of sympatholytics in hyperthyroidism (beta-blockers)

A

Controls tachycardia, HTN, A Fib

43
Q

KI mechanism

A

Inhibits hormone release, antagonizes TSH, inhibits peroxidase

44
Q

KI indications

A 
Prior to thyroid surgery
Radiation emergencies (block uptake of 131 I)
45
Q

KI adverse effects

A

Rashes, swollen salivary glands, headache

Can cross placenta and cause hypothyroidism

46
Q

Glucocorticoids mechanism

A

Interacts with receptors in cytoplasm, resulting in release of hsp90. This exposes the DNA binding domain and allows translocation to the nucleus, where they bind as homodimers.

47
Q

Mineralocorticoids mechanism

A

Act at the distal convoluted tubule and collecting duct, induce the synthesis of proteins that promote transepithelial Na transport

Increases the lumen-negative transepithelial voltage that drive K and H into the urine

Net result: Na retention and K/H excretion

48
Q

Adrenal steroid indications

A

Replacement therapy: Addison’s disease, ACTH deficiency, acute loss of adrenal function, congenital adrenal hyperplasia (CAH - hydroxylases essential for steroid synthesis are deficient resulting in hypersecretion of either mineralocorticoids or androgens occurs)

49
Q

21-hydroxylase deficiency

A

Low glucocorticoids and mineralocorticoids, high ACTH, high androgens

50
Q

11-hydroxylase deficiency

A

Low glucocorticoids, high ACTH, high mineralocorticoids and androgens

51
Q

Adrenal excess treatments: what suppresses ACTH, what suppresses synthesis, what is a receptor antagonist?

A

SS analogs (suppress ACTH), glucocorticoid synthesis inhibitors (metyrapone and ketoconazole), receptor antagonist (mifepristone RU-486)

52
Q

ACTH test for adrenal hypofunction

A

Exogenous ACTH will stimulate secretion if problem is secondary but not primary

53
Q

Metyrapone test for adrenal hypofunction

A

Metyrapone blocks 11-hydroxylase, leading to less glucocorticoids, which leads to less negative feedback, which should lead to more ACTH secretion

54
Q

Dexamethasone test for adrenal hyperfunction

A

Test whether the adrenal response is suppressible. Pituitary adenomas are suppressible with high levels, ectopic ACTH and cortisol-producing tumors are not suppressible.

55
Q

Antiinflammatory mechanism of glucocorticoids

A

Decrease synthesis of prostaglandins and inflammatory cytokines, decrease lymphocytes/monocytes/eosinophils/basoils, decrease antibody production and antigen processing, decrease scar formation

56
Q

Chemotherapeutic mechanism of glucocorticoids

A

Decreases lymphocytes, especially good for hematologic malignancies

57
Q

Pegvisomant

A

GH receptor antagonist

58
Q

Bromocriptine/cabergoline

A

Ergots, dopamine agonists

Suppress GH and PRL

Endocrine - Matt (23 decks)

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