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Pharmacology 4090 > Endo > Flashcards

Endo Flashcards

1
Q

Describe amine hormone synthesis

A

Hormones get stored for release; cells typically contain many granules filled with stored hormone

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2
Q

What are some amine hormones?

A

Catecholamines, thyroid hormone, releasing or stimulating hormones

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3
Q

Describe peptide-protein hormone synthesis

A

Stored for release; cells typically contain granules filled with stored hormone

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4
Q

Examples of peptide-protein hormones

A

Insulin, GH, gonadotropins, releasing or stimulating hormones

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5
Q

Describe steroid hormone synthesis

A

Produced when needed and released immediately because they are lipophilic; have delayed biological effects

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6
Q

Examples of steroid hormones

A

Sex steroids, corticosteroids, vitamin D, cholesterol precursor

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7
Q

Release patterns of endocrine hormones

A

Constitutive, stimulated, pulsation, circadian rhythm

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8
Q

Describe constitutive release pattern

A

Constant release of hormone

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9
Q

Describe stimulated release pattern

A

Released when stimulated by environment or CNS activity

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10
Q

Describe pulsatile release pattern

A

Released in pulses

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11
Q

Hormones that follow constitutive pattern

A

Insulin, cortisol, thyroxine

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12
Q

Hormones that are stimulated

A

Insulin, cortisol, thyroxine (?)

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13
Q

Hormones that are released in pulses

A

Hypothalamic releasing hormones

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14
Q

Hormones that follow circadian rhythms

A

Cortisol, thyroxine

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15
Q

How are hormone receptors relevant to pharmacology?

A

Key points of intervention; agonists and antagonists

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16
Q

Describe cell surface receptors

A

GPCRs; used by proteins, polypeptides, and amines because they are less lipophilic; cause intracellular signal transduction and rapid response

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17
Q

Describe nuclear/cytosolic receptors

A

Used by steroids and vitamin D and retinoic acid because these ligands are lipophilic; ligand binding causes transcription; response is delayed (hours later)

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18
Q

Traditional endocrine system

A

Hypothalamus-AP-target gland axes; gonads, thyroid, adrenal cortex; regulated by CBS feedback

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19
Q

Name the independent endocrine glands

A

Pancreas, posterior pituitary, parathyroids

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20
Q

Name the dispersed endo cells

A

IGFs from the liver, GI hormones, renin from kidney

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21
Q

Etiologies of pathway dysfunction

A

Hypersecretion, hyposecretion, inappropriate target tissue response

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22
Q

Hypersecretion etiology

A

Primary or secondary tutors

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23
Q

Hyposecretion etiology

A

Autoimmune dysfunction, genetics, surgery, atrophy, toxicity

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24
Q

Inappropriate response etiology

A

Abnormal receptor expression, mutated receptors, iatrogenic

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25
Q

Non-endo uses for glucocorticoids

A

Inflammation, allergy, septic shock, immunosuppression, hematologic malignancy

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26
Q

Alpha cells secrete ________, beta cells secrete ________

A

Glucagon; insulin

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27
Q

What controls insulin release?

A

increase: [Glucose], vagus, B2-adrenergic stimulation, leucine, arginine, gi hormones

Decrease: somatostatin, A-adrenergic stimulation

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28
Q

Process of insulin release

A

Glucose enters cell, ATP increases, ATP-K+ channel depolarizer cell, Ca2+ increases, insulin is released

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29
Q

Insulin receptor

A

Extracellular alpha and beta subunits with intracellular tyrosine kinase domain

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30
Q

Effects of insulin

A

*Anabolism
Increase glycogen storage in liver and muscle, increase fatty acid synthesis in liver, increase triglyceride synthesis in adipose, increase protein synthesis in muscle

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31
Q

Type 1 diabetes characteristics

A

Insulin deficiency, childhood or puberty onset, immune-mediated or idiopathic, coxsackievirus B1

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32
Q

Type 1 diabetes treatment

A

Insulin therapy

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33
Q

Type 2 diabetes characteristics

A

Insulin resistance and eventual insulin deficiency

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34
Q

Type 2 diabetes treatment

A

Lifestyle changes or oral hypoglycemic agents

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35
Q

What is lispro insulin?

A

Lysine and proline residues inverted so monomers are released quickly (fast acting)

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36
Q

What is aspart insulin?

A

One proline changed to aspartate so monomers are released quickly (fast acting)

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37
Q

What is NPH?

A

Protamine that modulates monomer release (intermediate acting)

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38
Q

What is Lente?

A

Zinc aggregate in acetate buffer so monomer is slowly released (intermediate acting)

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39
Q

What is glargine?

A

Replacement with glycine in A chain and arginines in B chain, plus high zinc concentration, causing very slow release and metabolism (long acting)

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40
Q

What is ultralente?

A

Suspension of high concentration of zinc aggregate in acetate buffer (long acting)

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41
Q

Types of insulin therapy

A

Basal-bolus or split-mixed (NPH + lispro or aspart mixed)

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42
Q

Complications of insulin therapy

A

Hypoglycemia or immunopathology

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43
Q

Types of oral hypoglycemics

A

Insulin secretagogues, insulin sensitizers, alpha glucosidase inhibitors, and incretins

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44
Q

Insulin secretagogues mechanism

A

Bind and inhibit ATP-K+ channel, leading to cell depolarization and insulin release ; caution with hypoglycemia

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45
Q

Types of insulin secretagogues

A

Sulfonylureas- longer acting so can use once daily but has risk of hypo
Meglitinides- rapid action, can use in combo with long- acting agents, causes less hypo

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46
Q

Insulin sensitizer mechanism

A

Increase sensitivity of peripheral cells to insulin but do not promote its release

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47
Q

Thiazolidinediones

A

Type of insulin sensitizer; ligand at ppar-gamma; regulate genes for lipid and glucose metabolism (glucose transporters);work downstream of insulin

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48
Q

Alpha glucosidase inhibitors

A

Inhibit alpha-glucosidases so digestion and absorption of starches decreases; can cause abdominal pain, diarrhea, flatulence

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49
Q

Incretins

A

Stimulated by glucose in intestine; tell the pancreas to increase insulin release

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50
Q

Types of incretins

A

Gastric inhibitory peptide (GIP) and glucagon like peptide 1 (GLP-1); very similar in structure and both N terminals are severed by DPP-4; get recognized by the pancreas to increase sensitivity

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51
Q

DPP-4 inhibitors

A

Inhibit the enzyme that inactivates incretins; could be used as an oral hypoglycemic to treat type 2 diabetes; sitagliptin

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52
Q

Biguanides

A

Type of insulin sensitizer; reduce hepatic gluconeogenesis and increase insulin utilization by peripheral cells; can use with secretagogues or insulin

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53
Q

Synthetic GLP-1

A

Liraglutide and exenatide

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54
Q

Liraglutide

A

Long-acting synthetic GLP-1 with fatty acid residue so it is bound to albumin and slowly released; decreases appetite and serum triglycerides but must be injected because it’s a peptide

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55
Q

Exenatide

A

GLP-1 agonist produced by gila monsters in saliva to rapidly activate beta cells and release insulin; may cause nausea, diarrhea, etc.

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56
Q

Glucagon

A

Hormone produced by alpha cells that opposes insulin; used in hypoglycemic emergency

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57
Q

Cortisol regulation

A

Hypothalamus is stimulated by stress, cold, etc. To release CRH, which causes ACTH release from the AP and results in cortisol synthesis from the adrenal cortex; negatively feeds back

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58
Q

Aldosterone regulation

A

Adrenal cortex is stimulated by ATII, potassium, and somewhat by ACTH

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59
Q

The zona glomerulosa releases

A

Aldosterone

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60
Q

The zona fasciculata releases

A

Primarily cortisol

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61
Q

The zona reticularis releases

A

Androgens and estrogen

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62
Q

Function of the renal juxtaglomerular apparatus

A

Monitors osmolarity and BP using macula densa and renin-secreting cells; when BP drops, renin increases

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63
Q

Action of renin

A

Produces angiotensin I

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64
Q

Effects of angiotensin II

A

Vasoconstriction and increased aldosterone secretion from adrenals

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65
Q

Rate limiting step of steroidogenesis

A

Conversion of cholesterol to pregnenolone by p450scc by knocking off the side chain

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66
Q

Key enzyme for glucocorticoid synthesis

A

P450c11, which hydroxylates carbon 11 so it can now bind the glucocorticoid receptor

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67
Q

Production of androgens

A

Pregnenolone follows a different conversion pathway to produce androstenedione

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68
Q

Production of aldosterone from pregnenolone

A

P450aldo adds additional groups to the molecule so it can now bind the mineralocorticoid receptor

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69
Q

Function of transcortin (CBG)

A

Carries cortisol in the blood stream and protects it from degradation until it reaches the target cell

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70
Q

How is aldosterone unique among the steroids?

A

It is almost completely unbound in the bloodstream

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71
Q

Actions of cortisol

A

Increase carb, lipid, and protein metabolism, as well as gluconeogenesis and glycogen synthesis in liver; inhibits production of proinflammatory mediators; short-term mood enhancement; vasoconstriction and CV support; stimulates fetal lung surfactant

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72
Q

Aldosterone actions

A

Fluid and electrolyte balance; promotes sodium reabsorption and proton/potassium excretion; maintains BP

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73
Q

Where aldosterone exerts effects

A

Distal tubule and collecting duct

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74
Q

3 categories of steroid preparations

A

Short-medium acting, intermediate acting, long-acting

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75
Q

Short-medium acting steroids

A

Cortisone, prednisolone, methylprednisolone

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76
Q

Intermediate-acting steroids

A

Triamcinolone

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77
Q

Long-acting steroids

A

Betamethasone, dexamethasone

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78
Q

Mineralocorticoid preparations

A

Fludricortisone, desoxycorticosterone; strong salt-retaining ability

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79
Q

What is fluticasone propionate (Flonase)

A

Topically active glucocorticoid that binds the corticosteroid receptor, but is hydrolyzed as soon as it hits the bloodstream and is inactivated; useful for asthma inhalers

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80
Q

What is mifepristone

A

Glucocorticoid and progesterone antagonist; binds receptor but prevents receptor folding

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81
Q

Cushing’s syndrome

A

Hyperadrenocorticism; buffalo hump, thin skin, muscle wasting at periphery, osteopenia, prone to infection, high BP

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82
Q

Causes of cushing’s syndrome

A

Pituitary adenoma (cushing’s disease), iatrogenic, ectopic ACTH syndrome, adrenal gland tumors

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83
Q

Diagnosis of cushing’s syndrome

A

Adrenal: elevated cortisol, low ACTH, glucocorticoid injection will do nothing
Pituitary: elevated ACTH, glucocorticoid injection will suppress ACTH

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84
Q

Adrenocorticosteroid inhibitors

A

Mitotane; inhibits production of cortisol

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85
Q

Corticosteroid synthesis inhibitors

A

Ketoconazole, aminoglutethimide, trilostane

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86
Q

Addison’s disease

A

Adrenal insufficiency; usually from autoimmune destruction of adrenals, can also be from abrupt steroid withdrawal or removal of adrenal or pituitary tumors

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87
Q

Acute adrenal insufficiency

A

Emergency; need IV fluid and corticosteroids

88
Q

Chronic adrenal insufficiency

A

Less severe; can use long-term glucocorticoid and mineralocorticoid replacement therapy

89
Q

Minimizing adverse effects of steroids

A

Use low dose and low potency steroids (prednisone), use alternate day therapy, taper reduction

90
Q

Mineralocorticoid antagonists

A

For primary aldosteronism (see hypertension and hypokalemia); spironolactone, eplerenone block the mineralocorticoid receptor

91
Q

3 forms of thyroid hormones

A

T4, T3, rT3

92
Q

3 deiodinases

A

D1, D2, D3

93
Q

D1 deiodinase action

A

Deiodinates both the inner and outer ring (produce T3, inactivate everything)

94
Q

D2 iodinase action

A

Deiodinates the outer ring (T4 —> T3 intracellularly)

95
Q

D3 iodinase action

A

Deiodinates the inner ring (inactivates T4 and T3)

96
Q

T4 production in thyroid

A

Tyrosine is iodinated by TPO and then these are combined to form T4. Thyroglobulin is then proteolyzed and release into the blood as either T4 or T3

97
Q

Ratio of t4 to t3

A

4:1

98
Q

Action of TBG

A

Bind thyroid hormone and greatly increase their half-life

99
Q

T3 is __________ as potent as T4

A

4 times

100
Q

Actions of thyroid hormones

A

Control transcription and translation of genes for metabolism; increase cellular oxygen use; allow for growth and development of tissues; increase myocardial contractile proteins

101
Q

Hypothyroidism etiology

A

Most commonly primary; can also be TSH insufficiency or iodine deficiency; gland absence; autoimmune thyroiditis (Hashimoto’s; AB’s against TPO); surgery, radioactive iodine; thioamides; chemo

102
Q

Hypothyroidism clinical signs

A

Lethargy, weakness, fatigue, cold intolerance, weightgain, Bradycardia, myxedema

103
Q

Goitrous hypothyroidism

A

From iodine deficiency, neoplasms, autoimmune destruction; causes gland growth

104
Q

Hypothyroidism diagnosis

A

Low T4, elevated TSH

105
Q

Levothyroxine

A

Synthetic T4; long half-life so you can take once daily, easily monitored, reaches steady-state in 6-8 weeks

106
Q

Liothyronine

A

T3; has shorter half-life so it is used much less

107
Q

Liotrix

A

Mixture of T4/T3 in 4:1 ratio; used for long-standing disease, in elderly, for CV disease, given in myxedema medical emergency

108
Q

Other treatments for hypothyroidism

A

Removal of drugs, iodine supplementation

109
Q

Hyperthyroidism ethology

A

Graves’ disease (antibodies activate TSH receptor), too much t4 supplementation, neoplasms, infection o inflammation of thyroid (transient)

110
Q

Clinical signs of hyperthyroidism

A

Hyperactive, nervous, insomnia, heat intolerance, tachycardia, weight loss, muscle wasting, exophthalmos

111
Q

Hyperthyroidism diagnosis

A

High T3/T4, low TSH, can use radioiodine uptake scan, MRI, or ultrasound

112
Q

Thioamides

A

Inhibit TPO so hormone synthesis is blocked; given orally

113
Q

Iodinated contrast medic

A

Inhibit conversion of t4 to t3 so there is less biological effect, but have short-term effects

114
Q

Adjunct drugs for hyperthyroidism

A

Beta blockers or calcium channel blockers

115
Q

Radioiodine therapy

A

Use i131- give orally and gets taken up by thyroid to destroy cells; some need second treatment, but most become hypo

116
Q

Thyroidectomy

A

Used for large glands or multinodular goiters;use antithyroid drugs pre-surgery; will need replacement t4 therapy after surgery

117
Q

Type of release of GNRH

A

Pulsatile (same with FSH and LH but less so)

118
Q

What is GNRH?

A

Decapeptide from hypothalamic neurofibers

119
Q

What releases FSH and LH

A

Anterior pituitary

120
Q

Effect of continuous release of GnRH

A

Down-regulation of the receptor

121
Q

What is inhibin?

A

Protein produced by sertoli cells and granulosa cells; inhibits FSH release selectively

122
Q

Action of FSH

A

Stimulates follicular development; converts androgen to estrogen j acts on sertoli cells to increase spermatogenesis

123
Q

Action of LH

A

Stimulates ovulation; produces androgens; regulates testosterone production

124
Q

Gonadorelin

A

Synthetic GnRH used in both sexes for hypogonadotrophic hypogonadism

125
Q

Leuprolide

A

Long-acting GnRH agonist used to induce hypogonadism; used for prostate cancer and hyperplasia, uterine fibroids, early puberty, assisted reproduction

126
Q

FSH analogues

A

human menopausal gonadotropins extracted from urine of postmenopausal women (have to use in conjunction with LH) ; recombinant FSH

127
Q

LH analogues

A

Human chorionic gonadotropins produced by placenta and excreted in urine; recombinant LH and hCG

128
Q

Where testosterone is produced

A

Leydig cells

129
Q

Testosterone synthesis

A

Comes from cholesterol and pregnenelone; converted to estradiol by aromatase and DHT by 5alpha-reductase in peripheral tissues

130
Q

What is TeBG

A

Testosterone binding globulin; carries 98% of testosterone in the blood

131
Q

DHT versus testosterone

A

DHT has higher affinity for the receptor

132
Q

Effects of androgens

A

Secondary sex characteristics; spermatogenesis, deepening of voice, facial hair, libido, behaviorer, body mass, erythropoiesis, decreased HDL, growth plate closure

133
Q

Testosterone preparations

A

1:1 androgen: anabolic effect

134
Q

Long-acting testosterone analogues

A

Have a longer half-life due to ester addition

135
Q

Side effects of androgen preparations

A

Prostate enlargement, aggression, hepatic dysfunction, sterility, heart disease, masculinization of women

136
Q

Androgen replacement therapy

A

Replaces or augments androgens in hypogonadal men; use testosterone

137
Q

Uses for androgens and anabolic steroids

A
  1. Androgen replacement therapy
    2.Gynecologic disorders
  2. Use as protein anabolic agent
  3. Growth stimulators and aging
  4. Steroid abuse
138
Q

Danazol

A

Weak synthetic androgen used in endometriosis that inhibits estrogen-induced growth of endometrial tissue

139
Q

Uses for Anti androgens

A

For prostatic cancer, benign prostatic hyperplasia, endometriosis, male pattern baldness, excessive sex drive, early puberty in men

140
Q

Ways to suppress androgen action

A
  1. GnRH agonists (leuoprolide)
  2. Testosterone synthesis inhibitors (ketoconazole, spironolactone)
  3. Inhibition of 5alpha-reductase (finasteride)
  4. Androgen receptor antagonists (flutamide, cyproterone)
141
Q

Estrogen synthesis in premenopausal women

A

Estradiol mostly, produced by ovary

142
Q

Steroidal estrogens

A

From testosterone or androstenedione in ovaries, converted to estrogen via aromatase

143
Q

Estriol

A

Synthesized from estradiol in liver, as well as in placenta during pregnancy

144
Q

Estrogen synthesis in post menopausal women

A

From adipose tissue, adrenals also produce estrone

145
Q

Estrogen synthesis in men

A

Extra-gonadal conversion of testosterone, DHEA, and androstenedione

146
Q

Synthetic estrogens

A

Ethinyl estradiol, diethylstilbesterol

147
Q

Progestin meaning

A

Any steroid with progesterone activity

148
Q

Progesterone

A

Most important natural progestin in women,produced in ovaries, adrenals, and placenta; can be precursor for estrogens, androgens, and adrenocorticoids

149
Q

Synthetic progestins

A

L-norgestrel, norethidrone, medroxyprogesterone

150
Q

Progestins in men are produced where?

A

Produced in testes

151
Q

Estrogen binds to ______ in the blood stream, while progesterone binds to ______

A

TeBG; CBG

152
Q

Estrogen receptor types

A

Alpha and beta

153
Q

Effects of estrogens

A

Sexual maturation, sense of well-being, ovulation, parturition, endometrial growth, reduced resorption of sone, increased clotting factors, growth, epiphysis closure

154
Q

Effects of progesterone

A

Modulates carb metabolism, suppresses ovulation, deposits adipocytes, sexual maturation, behaviour, mood

155
Q

Uses for estrogens, progestins, and gonadal inhibitors

A
  1. Fertility control (Post-coital contraception, Contragestation)
  2. Hormone replacement therapy
  3. Ovulation induction
  4. Cancer chemo
156
Q

Post-coital contraception

A

Large dose of estrogen alone or with progestin; prevents implantation; must be taken within 72 hours

157
Q

Contragestation

A

Mifepristone; antiprogestin that blocks progesterone receptor so implantation cannot occur and endometrium is shed; usually given with prostaglandin for contraction

158
Q

Two types of oral contraceptives

A

Combination of Estrogen and progestins or continuous therapy of only progestins

159
Q

Combined oral contraceptives

A

Ethinylestradiol plus l-norgestrel or norethindrone; can vary levels of progestin throughout 28 day cycle; inhibits ovulation because estrogen and progestin inhibit gonadotropin release; thickens cervical mucus; progestins protect endometrium

160
Q

Progestin-only mini pill

A

Slightly higher failure, higher incidence of menstrual irregularity; contains either norgestrel or norethindrone; still inhibits cycle and thickens mucus

161
Q

Alternative contraceptives

A

Norplant-2 placed subcutaneously in arm, medroxyprogesterone intramuscular injections, progesterone IUDs

162
Q

2 uses for estrogen or progesterone replacement therapy

A

Congenital primary hypogonadism, menopause/surgical removal of ovaries

163
Q

Treatment for congenital primary hypogonadism

A

Low dose estrogen for most of month and then progestin to initiate uterine bleeding

164
Q

Treatment for menopause/surgical removal of ovaries

A

Estrogens and progestins to antagonize estrogen effects on endometrium

165
Q

Symptoms of menopause or ovarectomy

A

Atrophy of genitalia, depression, loss of libido, lack o energy, hot flashes (vasomotor spasm), osteoporosis, cardiovascular disease

166
Q

Drugs for ovulation induction

A

GnRH analogues it pituitary is functioning, gonadotropins if ovary is functioning; clomiphene citrate

167
Q

Clomiphene citrate

A

Partial agonist/antagonist at estrogen receptor that decreases estrogen to stop negative feedback on hypothalamus/pituitary → increases FSH → increased follicles; repeat every cycle (SERM)

168
Q

Drugs for cancer chemo

A

Diethylstilbesterol for prostate cancer, selective estrogen receptor modulators, estrogen synthesis inhibitors

169
Q

Selective estrogen receptor modulators

A

Selectively antagonize certain estrogen receptors; used for treatment of breast cancer but have low risk of osteoporosis

170
Q

Estrogen synthesis inhibitors

A

Aromatase inhibitors that function everywhere in the body so they’re more effective for breast cancer but have higher risk of osteoporosis; can use with tamoxifen

171
Q

Mild effects of estrogens and progestins

A

Nausea, headaches, endocrine changes

172
Q

Moderate effects of estrogens and progestins

A

Weight gain, vaginal and uterine tract infections, bleeding, depression

173
Q

Severe effects of estrogens and progestins

A

Hepatic dysfunction, cancers (breast, endometrial) thromboembolic disease, MI, hypertension, stroke, concern with other risk factors

174
Q

Oxytocin structure

A

Nonapeptide

175
Q

Oxytocin synthesis

A

In paraventricular nuclei and supraoptic nuclei, secreted from nerve endings, also synthesized in luteal cells of ovary, uterus, and fetus

176
Q

Oxytocin stimulation

A

Sensation from cervix and vagina, suckling

177
Q

Effects of oxytocin

A

Increases frequency and force of uterine contractions, stimulates milk ejection

178
Q

Hormones needed for oxytocin to work

A

Estrogen for contractions, prolactin for milk formation

179
Q

Hormone that antagonizes oxytocin

A

Progesterone; necessary to prevent premature labour

180
Q

Pitocin

A

Synthetic oxytocin given intravenously to induce labour or by nasal spray for postpartum lactation

181
Q

Contraindications for oxytocin administration

A

Fetal distress, premature labor, abnormal fetal positioning, cephalopelvic disproportion

182
Q

Atosiban

A

Oxytocin antagonist used for premature labour (not used in NA)

183
Q

What is vasopressin

A

Nonapeptide from posterior pituitary that acts as ADH

184
Q

Stimuli for vasopressin

A

Increasing toxicity by osmoreceptors, BP drop by baroreceptors

185
Q

Actions of vasopressin

A

Promotes water retention via v2 receptors, constricts vessels via v1 receptors

186
Q

Synthetic vasopressin types

A

Vasopressin, desmopressin (long-acting, no vasoconstriction)

187
Q

Uses for synthetic vasopressin’s

A

Pituitary diabetes insipidus, nocturnal enuresis

188
Q

What electrolytes regulate bone homeostasis

A

Calcium and phosphate

189
Q

Effects of bone abnormalities

A

Neuromuscular excitability, weakness, tetany, joint malfunction, decreased hematopoiesis

190
Q

Effects of PTH

A

Increases serum calcium, decreases serum phosphate

191
Q

Effects of vitamin D

A

Increases both serum calcium and phosphate; directly suppresses PTH production

192
Q

Effects of calcitonin

A

Lowers serum calcium and phosphate; inhibits osteoclasts

193
Q

Effect of estrogen on bones

A

Inhibit osteoclasts; slow bone turnover; increases vitamin D

194
Q

What is osteoporosis

A

Low bone mass in long bones

195
Q

Primary osteoporosis

A

Loss of estrogen production in postmenopausal women (and older men)

196
Q

Osteoporosis risk factors

A

Female, Caucasian, smoking, fracture, age, low weight, family history

197
Q

Secondary osteoporosis

A

From diet, gi disease, hyperparathyroidism, liver disease, alcoholism, vitamin D deficiency, corticosteroid use

198
Q

Primary regulators of bone mass

A

Physical activity, calcium intake, reproductive statues

199
Q

Therapies for osteoporosis

A

SERMs, bisphosphonates, PTH analogues, calcitonin, vitamin D

200
Q

SERMs for osteoporosis

A

Raloxifene; Estrogen agonist in bone, antagonist in breast and uterus, doesn’t prevent hot flashes

201
Q

Bisphosphonates

A

Most successful therapy; inhibit osteoclast function

202
Q

PTH analogues

A

Recombinant PTH, stimulates bone formation at low doses

203
Q

Calcitonin therapy

A

Inhibits osteoclasts

204
Q

Vitamin D therapy

A

Improves intestinal calcium absorption to improve mineral density

205
Q

Negative and positive stimuli for gh

A

Negative: somatostatin, positive: growth hormone releasing hormone

206
Q

Effects of GH

A

Stimulates synthesis and release of IGF-1 from liver and growth plate; promotes lipolysis, gluconeogenesis, and protein synthesis, as well as skeletal and soft tissue growth

207
Q

Causes of GH deficiency

A

Genetics, hypothalamus problem or pituitary problem

208
Q

Signs of GH deficiency

A

Cardio problems, psychosocial problems, decreased muscle and bone mass, increased fat, less energy, poor libido

209
Q

Diagnosis of gh deficiency

A

Measurement of serum gh levels

210
Q

Gh deficiency treatments

A

Recombinant GH, rhIGF1/rhIGFBP3 for receptor defects of GH antibodies, synthetic GHRH (not if issue is at pituitary)

211
Q

Effect of excess gh

A

Gigantism when young, acromegaly in adulthood

212
Q

Signs of acromegaly

A

Soft tissue overgrowth, elevated serum IGF1 or GH

213
Q

Therapies for gh excess

A

Ocreotide (somatostatin analogue) , pegvisomant (GH antagonist)

214
Q

What is prolactin

A

Peptide hormone from ap that causes breast development and milk production

215
Q

Effects of excess prolactin

A

Inappropriate breast development and lactation, reproductive difficulties

216
Q

Effect of dopamine on prolactin

A

Decreases prolactin secretion from pituitary

217
Q

Bromocriptine and cabergolide

A

Stimulates d2 receptors in ap to decrease prolactin; used for prolactinomas, acromegaly; can give orally or intravaginally

Pharmacology 4090 (11 decks)

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