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Pharmacology > VI-Topnotch-Pharma-Flash-Cards-Endocrine-Drugs > Flashcards

VI-Topnotch-Pharma-Flash-Cards-Endocrine-Drugs Flashcards

1
Q

Recombinant Growth hormone

A

Somatropin (TOPNOTCH)

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2
Q

Increases release of IGF-1 in the liver and carilage, stimulates skeletal muscle growth, amino acid transport, protein synthesis and cell proliferation

A

Somatropin (TOPNOTCH)

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3
Q

Recombinant IGF-1

A

Mecasermin (TOPNOTCH)

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4
Q

Somatostatin analog

A

Octreotide, Lanreotide (TOPNOTCH)

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5
Q

suppresses the release of growth hormones, glucagon, insulin, gastrin, IGF-1, serotonin and gastrointestinal peptides

A

Octreotide, Lanreotide (TOPNOTCH)

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6
Q

For Acromegaly, pituitary adenoma, carcinoid, gastrinoma, glucagonoma, variceal bleeding

A

Octreotide, Lanreotide (TOPNOTCH)

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7
Q

GH receptor antagonist ; For acromegaly

A

Pegvisomant (TOPNOTCH)

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8
Q

Gonadotropin analog (FSH analog) ; For Controlled ovarian hyperstimulation, infertility due to hypogonadism in men

A

Follitropin alfa, Follitropin beta, Urofollitropin (TOPNOTCH)

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9
Q

Gonadotropin analog (LH analog)

A

For Controlled ovarian hyperstimulation (ovulation induction), hypogonadotripic hypogonadism (TOPNOTCH)

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10
Q

SE: Headache, depression, edema, ovarian hyperstimulation syndrome, multiple pregnancies in women, gynecomastia in men

A

FHS and LH analogs (TOPNOTCH)

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11
Q

GnRH analog

A

Leuprolide, Gonadorelin, Goserelin, Histrelin, Nafarelin, Triptorelin (TOPNOTCH)

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12
Q

For Controlled ovarian hyperstimulation, endometriosis, myoma uteri, precocious puberty, postate CA

A

Leuprolide, Gonadorelin, Goserelin, Histrelin, Nafarelin, Triptorelin (TOPNOTCH)

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13
Q

there is exacerbation of symptoms in males with prostate CA and children with precocious puberty during the first few weeks of therapy

A

GnRH analog (TOPNOTCH)

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14
Q

For GnRH analogs: increased LH and FSH secretion with ________ administration , reduced LH and FSH secretion with ________ administration

A

intermittent ; prolonged continuous (TOPNOTCH)

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15
Q

GnRH antagonist

A

Ganirelix, Cetrorelix, Degarelix (TOPNOTCH)

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16
Q

For Controlled ovarian hyperstimulation (prevents premature LH surge), advanced prostate CA

A

Ganirelix, Cetrorelix, Degarelix (TOPNOTCH)

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17
Q

Does NOT cause tumor flare-up whe used for treatment of advanced prostate cancer

A

Ganirelix, Cetrorelix, Degarelix (TOPNOTCH)

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18
Q

_____ is used for prostate CA while _____ prevent LH surge in controlled ovulation

A

Degarelix ; Ganirelix (TOPNOTCH)

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19
Q

Dopamine agonist, partial agonist at dopamine D2 receptors in brain ; For Hyperprolactinemia, Pituitary adenoma, acromegaly, Parkinson’s disease

A

Bromocriptine, Carbegoline (TOPNOTCH)

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20
Q

Activates oxytocin receptors stimulates uterine contraction and labor, stimulates mammary glands, lactation and milk let-down

A

Oxytocin (TOPNOTCH)

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21
Q

For Labor induction, labor augmentation, control of uterine hemorrhage post-delivery

A

Oxytocin (TOPNOTCH)

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22
Q

oxytocin antagonist used in preterm labor

A

ATOSIBAN (TOPNOTCH)

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23
Q

ADH agonist, Vasopressin V2 receptor agonist

A

Desmopressin (TOPNOTCH)

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24
Q

For Central DI, Hemphilia A, von Willebrand’s disease, Variceal bleeding, primary nocturnal seizures

A

Desmopressin (TOPNOTCH)

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25
Q

SE: Fetal distress, placental abruption, uterine rupture, fluid retention, hyponatremia, heart failure, seizures, hypotension

A

Oxytocin (TOPNOTCH)

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26
Q

ADH antagonist, Antagonist at V1a and V2 receptors

A

Conivaptan, Tolvaptan (TOPNOTCH)

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27
Q

_____ may occur with rapid correction of hyponatremia

A

Central pontine myelinolysis (TOPNOTCH)

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28
Q

Which is more selective for V2 receptors, Conivaptan or Tolvaptan?

A

tolvaptan (TOPNOTCH)

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29
Q

Thryoid hormone ; For Hypothyroidism, myxedema coma

A

Levothyroxine (T4), Liothyronine (T3) (TOPNOTCH)

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30
Q

T or F: Liothyronine has a faster onset but shorter half-life

A

TRUE (TOPNOTCH)

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31
Q

Inhibits thyroid peroxidase reactions, blocks iodine organification, inhibits peripheral conversion of T4 into T3

A

Propylthiouracil (PTU) (TOPNOTCH)

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32
Q

Drug of choice for pregnant hyperthyroid patients

A

Propylthiouracil (PTU) (TOPNOTCH)

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33
Q

Inhibits thyroid peroxidase reactions, blocks iodine organification

A

Methimazole, Carbimazole (TOPNOTCH)

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34
Q

Inhibit iodine organification and hormone release leading to reduced size and vascularity of thyroid gland

A

Lugol Solution (Iodine in Potssium Iodide), Potassium Iodide (TOPNOTCH)

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35
Q

onset is more rapid (2-7 days) but effect is transient ; Should not be used alone (escape in 2-8 weeks); prevents radiation induced thryoid damage; prenatal exposure causes fetal goiter

A

Lugol Solution (Iodine in Potssium Iodide), Potassium Iodide (TOPNOTCH)

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36
Q

Beta blocker control HR and other cardiac abnormalities of severe thyrotoxicosis, slows pacemaker activity; inhibits peripheral conversion of T4 into T3

A

Propranolol, Esmolol, Metoprolol, Atenolol (TOPNOTCH)

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37
Q

_____ may be used to treat thyrotoxicosis-related arrhythmias

A

Esmolol (TOPNOTCH)

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38
Q

Iodide, emits beta rays causing destruction of thyroid parenchyma

A

Radioactive Iodine (TOPNOTCH)

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39
Q

For hyperthyroidism, permanent cure of thyrotoxicosis without surgery and no effect on other tissues

A

Radioactive Iodine (TOPNOTCH)

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40
Q

Preferred treatment for most patients due to ease of administration, effectiveness, low expense and absence of pain; contraindicated in pregnant women or nursing mothers

A

Radioactive Iodine (TOPNOTCH)

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41
Q

Low Potency Glucocorticoid (GC)

A

Desonide (TOPNOTCH)

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42
Q

Medium Potency GC

A

Fluticasone, Mometasone (TOPNOTCH)

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43
Q

High Potency GC

A

Desoximetasone, Clobetasol (TOPNOTCH)

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44
Q

Effects: stimulate gluconeogenesis, increased fat deposition, protein catabolism, inhibit cell-mediated immunologic functions, lymphotoxic, increased neutrophils, decreased lymphocytes, eosinpphils, basophils and monocytes, inhibit leukocyte migration, inhibit PLA2

A

Glucocorticoids (TOPNOTCH)

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45
Q

_____ is the active metabolite of prednisone

A

prednisolone (TOPNOTCH)

46
Q

SE: Adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, behavioral changes (psychosis)

A

Glucocorticoids (TOPNOTCH)

47
Q

For supressession of inflammation and immune response, hematopoeitic cancers, transplant rejection, collagen and rheumatic disease, lung maturation in preterm labor

A

Glucocorticoids (TOPNOTCH)

48
Q

strong agonist of mineralocorticoid receptors and moderate activation of glucorticoid receptors

A

Mineralocorticoid (TOPNOTCH)

49
Q

Increases Na reabsorption, K and H excretion ; For Chronic adrenal insufficiency (Addison’s disease), Congenital adrenal hyperplasia, adrenal replacement therapy post-adrenalectomy

A

Mineralocorticoid (TOPNOTCH)

50
Q

Mineralocorticoid

A

Fludrocortisone, Deoxycorticosterone (TOPNOTCH)

51
Q

Additive hypokalemia with loop diurectics and thiazides

A

Fludrocortisone, Deoxycorticosterone (TOPNOTCH)

52
Q

Glucorticoid synthesis inhibitor, inhibits desmolase activity, blocking conversion of cholesterol to pregnenolone

A

Aminoglutethimide (TOPNOTCH)

53
Q

Glucorticoid synthesis inhibitor, inhibits cholesterol side chain cleavage, cytochrome P450 enzymes and other enzymes necessary for synthesis of all steroids

A

Ketoconazole (TOPNOTCH)

54
Q

Ketoconazole is CYP450 inhibitor or inducer?

A

Inhibitor (TOPNOTCH)

55
Q

Glucorticoid synthesis inhibitor, selective inhibitor of steroid-11 hydroxylation

A

Metyrapone (TOPNOTCH)

56
Q

DOC for pregnant patients with Cushing’s syndrome

A

Metyrapone (TOPNOTCH)

57
Q

competitive inhibitor at the GC receptor as well as progesterone receptor ; For Cushing’s syndrome

A

Mifepristone (RU486) (TOPNOTCH)

58
Q

also used as an approved abortifacient for medical abortion (usually together with misoprostol)

A

Mifepristone (RU486) (TOPNOTCH)

59
Q

Activates etrogen receptors, leads to changes in rates of trasncription of estrogen-regulated genes

A

Estrogens: Ethinyl Estradiol, Mestranol, Estradiol cypionate, Premarin (TOPNOTCH)

60
Q

Synthetic estrogen (nonsteroid); activates estrogen receptors; leads to changes in rates of transcription of estrogen-regulated genes ; For Atrophic vaginitis, hormone replacement therapy, prevention of adverse pregnancy outcomes, metastatic prostate CA

A

Diethylstilbestrol (TOPNOTCH)

61
Q

associated with Infertility, ectopic pregnancy, clear cell vaginal adenocarcinoma in daughters of women who used this drug

A

Diethylstilbestrol (TOPNOTCH)

62
Q

activates progesterone receptors, change rates of transcription of progesterone-regulated genes ; For Hormone replacement therapy, contraception, assisted reproduction, anovulation induction

A

Progestins: Norgestrel, Medroxyprogesterone, Norethindrone, Norgestimate, Desogestrel,Megestrol (TOPNOTCH)

63
Q

IM depot preparation

A

Medroxyprogesterone Acetate (TOPNOTCH)

64
Q

Must be taken within 72 hours of unprotected sexual intercourse

A

Levonorgestrel (TOPNOTCH)

65
Q

Estrogen antagonist actions in breast tissue and CNS, Estrogen agonist effects in uterus, liver and bone

A

Tamoxifen, Torimefene (TOPNOTCH)

66
Q

Estrogen antagonist actions in breast tissue, uterus, and CNS, Estrogen agonist effects in liver and bone

A

Raloxifene (TOPNOTCH)

67
Q

Partial agonist in pituitary, reduces negative feedback by estradiol, increases FSH and LH output, For Induction of ovulation

A

Clomiphene (TOPNOTCH)

68
Q

Reduces estrogen synthesisby inhibiting aromatase ; For breast CA, precocious puberty

A

Anastrozole, Letrozole, Exemestane (TOPNOTCH)

69
Q

Ovarian inhibitor, weak cytochrome P450 inhibitor and partial agonist of progestin and androgen receptors ; For Endometriosis, Fibrocystic disease, Hemophilia, Angioneurotic edema

A

Danazol (TOPNOTCH)

70
Q

Activates androgen receptors, promotes development of male characteristics, increases body muscle bulk and RBC production

A

Androgens: Testosterone, Fluoxymesterone, Methyltestosterone (TOPNOTCH)

71
Q

Effects: induces secretory changes in the endometrium, stabilize the endometrium, affect carbohydrate metabolism and stimulate deposition of fat, high doses suppress FSH and LH secretion

A

progesterone (TOPNOTCH)

72
Q

Effects: secondary sexual characteristics, fertility and libido, male pattern baldness, increases muscle mass, increased RBC production, decreased urea nitrogen excretion

A

Androgens: Testosterone, Fluoxymesterone, Methyltestosterone (TOPNOTCH)

73
Q

anabolic steroids

A

Oxandrolone, Stanozolol, Nandrolone (TOPNOTCH)

74
Q

Competitive antagonist at androgen receptor ; For Prostate CA, surgical castration

A

Flutamide, Bicalutamide, Nilutamide (TOPNOTCH)

75
Q

Antagonist at androgen receptor. Marked progestational effect that suppresses the feedback enhancement of LH and FSH

A

Cyproterone (TOPNOTCH)

76
Q

Androgen synthesis inhibitor, inhibits 5a reducase enzyme that converts testosterone to dihydrotestosterone ; For BPH, Male pattern baldness. Hirsutism

A

Finasteride, Dutasteride (TOPNOTCH)

77
Q

Activates a Tyrosine Kinase typer of receptorsleading to a reducting of circulating glucose: promotes glucose transport and oxidation; glycogen, lipid, protein synthesis and regulation of gene expression

A

Insulin (TOPNOTCH)

78
Q

Rapid Acting Insulin

A

Lispro, Aspart, Glulisine (TOPNOTCH)

79
Q

Short Acting Insulin

A

Regular Insulin (TOPNOTCH)

80
Q

Intermediate Acting Insulin

A

NPH, Lente (TOPNOTCH)

81
Q

Long Acting Insulin

A

Detemir, Glargine, Ultralente, Lantus (TOPNOTCH)

82
Q

peakless insulins

A

Long Acting Insulin (TOPNOTCH)

83
Q

acts as an insulin secretagogue, increases insulin secretion from pancreatic beta cells by closing ATP sensitive K+ channels leading to depolarization of the B cell

A

Sulfonylureas (TOPNOTCH)

84
Q

2nd generation sulfonylurea

A

Glipizide, Glibenclamide, Glimepiride, Gliclazide, Glyburide (TOPNOTCH)

85
Q

1st generation sulfonylurea

A

Tolazamide, Tolbutamide, Chlorpropamide (TOPNOTCH)

86
Q

T or F: 1st gen SUs have less hypoglycemia than 2nd gen

A

FALSE (TOPNOTCH)

87
Q

Insulin Secretagogue, similar to sulfonylureas with some overlap in binding sites, reduces circulating glucose, increases glycogen, fat and protein formation and gene regulation

A

Meglitinides (TOPNOTCH)

88
Q

Meglitinides

A

Repaglinide, Nateglinide (TOPNOTCH)

89
Q

Least hypoglycemia among OHAs

A

Meglitinides (TOPNOTCH)

90
Q

Reduced hepatic and renal gluconeogenesis with decreased endogenous glucose production, activates AMP-stimulated protein kinase leading to inhibition of gluconeogenesis

A

Biguanides (TOPNOTCH)

91
Q

Biguanides

A

Metformin (TOPNOTCH)

92
Q

DOC for obese diabetics

A

Metformin (TOPNOTCH)

93
Q

Inhibits intestinal alpha-glucosidases , reduces conversion of starch and disacchardies to monosaccharidea, reduces post prandial hyperglycemia

A

Alpha Glucosidase Inhibitors (TOPNOTCH)

94
Q

Alpha Glucosidase Inhibitors

A

Acarbose, Miglitol (TOPNOTCH)

95
Q

Regulates gene expression by binding to PPAR-gamma and PPAR-alpha which increases tissue sensitivity, increases glucose uptake in muscle and adipose tissue, inhibits hepatic gluconeogenesis, effects on lipid metabolism and distribution of body fat, control of fasting and postprandial glucose, decreased risk of DM in high-risk patients

A

Thiazolidinediones (TOPNOTCH)

96
Q

Thiazolidinediones

A

Pioglitazone, Rosiglitazone (TOPNOTCH)

97
Q

binds to PPAR-gamma and PPAR-alpha

A

Pioglitazone (TOPNOTCH)

98
Q

binds to PPAR-gamma ONLY

A

Rosiglitazone (TOPNOTCH)

99
Q

SE: Fluid retention, weight gain, congestive heart failure, fractures esp in women, cardiovascular events, hepatotoxicity, macular edema, dyslipidemia, increased risk of MI

A

Thiazolidinediones (TOPNOTCH)

100
Q

Analog of GLP-1, Binds to GLP-1 receptors which leads to reducetion of post-meal glucose excursions, increases glucose-mediated insulin release, lowers glucagon levels, slows gastric emptying time, produces satiety

A

Exenatide (TOPNOTCH)

101
Q

Dipeptidyl Peptidase-4 Inhibitors, blocks degradation of GLP-1, raises circulating GLP-1 levels, reduces post-meal glucose excursions, increases glucose mediated insulin release, lowers glucagon levels, slows gastric emptying time, decreases appetite

A

Sitagliptin, Linagliptin (TOPNOTCH)

102
Q

Analog of amylin, Binds to amylin receptors, reduce post-meal glucose excursions, lowers glucagon levels, slows gastric emptying, decreases appetite

A

Pramlintide (TOPNOTCH)

103
Q

Bile acid binder, lowers glucose through unknown mechanisms

A

Colesevelam hydrochloride (TOPNOTCH)

104
Q

INACTIVE Vitamin D

A

Cholecalciferol, Ergocalciferol (TOPNOTCH)

105
Q

ACTIVE Vitamin D

A

Calcitriol, Doxercalciferol, Paricalcitol, Calcipotriene (TOPNOTCH)

106
Q

Suppress the activity of osteoclasts in part via inhibition of farnesyl pyrophosphate synthesis, inhibit resorption and formation of bone by acting on the basic hydroxyapatite crystal structure

A

Bisphosphonates (TOPNOTCH)

107
Q

Bisphosphonates

A

Alendronate, Risedronate, Ibandronate, Pamidronate, Zoledronate, Etidronate, Tiludronate, Zoledronic acid (TOPNOTCH)

108
Q

Recombinant PTH, Acts via cognate G protein coupled receptors, stimulates bone formation when given in low intermittent doses

A

Teriparatide (TOPNOTCH)

109
Q

Acts via cognate G protein coupled receptors; suppresses bone resorption ; For Paget’s disease of the bone, hypercalcemia, osteoporosis, tumor marker for thyroid CA

A

Calcitonin (TOPNOTCH)

110
Q

Interacts selectively with estrogen receptors, inhibits PTH-stimulated bone resorption without stimulating breast or endometrial hyperplasia, delay bone loss in post-menopausal women

A

Raloxifene (TOPNOTCH)

111
Q

Monoclonal antibody, binds to RANKL and prevents it from stimulating osteoclast differentiation and function, blocks bone resorption

A

Denosumab (TOPNOTCH)

112
Q

Activates the calcium sensing receptors in the parathyroid gland, inhibits PTH secretion

A

Calcium Receptor Antagonist: Cinacalcet (TOPNOTCH)

Pharmacology (8 decks)

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