Endo/ReproDrugs

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bshin
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84676
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Endo/ReproDrugs
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2011-06-14 03:18:46
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Endo Repro Drugs
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Endo/Repro Drugs
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  1. Treatment strategy for DM-1
    • low-sugar diet
    • insulin replacement

    • DM-1
    • early onset
    • loss of beta cells-->absolute dependence on insulin
    • ketoacidosis prone!
  2. Treatment strategy for DM-2
    • diet modify
    • exercise (lose weight)
    • oral hypoglycemics
    • insulin replacement

    • DM-2
    • adult onset
    • decrease response to insulin--> diet-->oral hypoglycemics +/- insulin
    • NOT ketoacidosis prone! more Hyperosmolar coma from hyperglycemia
  3. Insulin release increased by:
    • Glucose
    • Sulfonylureas
    • M-agonists
    • B2-agonists
  4. Insulin release decreased by:
    Alpha-2 agonists
  5. Mechanism of Insulin binding
    • Bind insulin receptor (RTK)--> autophosphorylate tyr-kinase--> bind/ phosphorylate IRS-1--> bind/phosphorylate SH2-domain proteins-->-->
    • activate phosphatases, induce gene expression of LPL, FA-sythase, Glucokinase...
  6. Lispro (Novolog)
    • rapid acting insulin (IV!)
    • -bind insulin receptor
    • -Liver: increase glucose stored as glycogen
    • -Muscle: increase glycogen synthesis, K+ uptake
    • -Fat: increase TG storage

    • USE- DM-1, DM-2
    • life-threatening hyperkalemia
    • stress induced hyperglycemia

    SE- hypoglycemia
  7. Regular
    • rapid acting insulin (IV)
    • -bind insulin receptor
    • -Liver: increase glucose stored as glycogen
    • -Muscle: increase glycogen synthesis, K+ uptake
    • -Fat: increase TG storage

    • USE- DM-1, DM-2
    • life-threatening hyperkalemia
    • stress induced hyperglycemia

    SE- hypoglycemia
  8. Aspart (Apidra, Humalog)
    • rapid acting insulin
    • -bind insulin receptor
    • -Liver: increase glucose stored as glycogen
    • -Muscle: increase glycogen synthesis, K+ uptake
    • -Fat: increase TG storage

    • USE- DM-1, DM-2
    • life-threatening hyperkalemia
    • stress induced hyperglycemia

    SE- hypoglycemia
  9. NPH
    • intermediate acting insulin
    • -bind insulin receptor
    • -Liver: increase glucose stored as glycogen
    • -Muscle: increase glycogen synthesis, K+ uptake
    • -Fat: increase TG storage

    • USE- DM-1, DM-2
    • life-threatening hyperkalemia
    • stress induced hyperglycemia

    SE- hypoglycemia
  10. Glargine
    • long acting insulin analog
    • -NO peak!
    • -supply constant background level insulin
    • -NO risk of hypoglycemia

    USE-DM-1, DM-2(?)
  11. Detemir (Levemir)
    • long acting insulin analog
    • -NO peak!
    • -supply constant background level insulin
    • -NO risk of hypoglycemia

    USE-DM-1, DM-2(?)
  12. Diabetic ketoacidosis
    • Ketones: (made from high ATP from burning fat)
    • beta-hydroxybutyric acid--> NADH + 2 acetyl-CoA
    • acetoacetate--> 2 acetyl-CoA
    • acetone--> breath out (fruity breath)

    • Symptoms:
    • -polyuria, polydipsia
    • -nausea, fatigue
    • -Kussmaul breathing (wanna rid of acidosis!)
    • -dehydration
    • -elevated serum K+, low intracellular K+ (b/c acidosis, and low insulin)

    • Rx- IV regular Insulin!
    • -give w/ glucose to prevent hypoglycemia
    • -give w/ K+ to prevent hypokalemia!!
  13. Hypoglycemic symptoms
    • lip/tongue tingling
    • lethargy
    • confusion
    • sweat
    • tremor
    • tachycardia
    • coma
    • seizures

    • RX- oral glucose, IV-dextrose (if unconscious)
    • glucagon (IM or inhalation)
    • - IM glucagon in non-medical setting, or IV dextrose in medical setting. but NOT IM-glucose!
  14. Mechanism of insulin release from pancreas
    eat-->glucose--> go thru GLUT-2 (low affinity) in pancreas beta cell--> increase ATP--> close ATP-dependent K-channel--> depolarize--> open vol-Ca channel--> Ca in--> exocytosis of insulin
  15. Acetohexamide
    • first gen Sulfonylurease (secretologue)
    • -close ATP-dep K channel in beta cells--> depol--> Ca influx--> insulin release
    • -decrease glucagon release
    • -increase insulin receptor sensitivity (?)
    • (useless in DM-1)

    USE-DM-2

    • SE- long acting!! watch out in renal disease pt
    • -weight gain, hypoglycemia
    • -drug interactions w/ Cimetidine (induce cyps), Salicylates, Sulfonamides
  16. Tolbutamide
    • first gen Sulfonylurease (secretologue)
    • -close ATP-dep K channel in beta cells--> depol--> Ca influx--> insulin release
    • -decrease glucagon release
    • -increase insulin receptor sensitivity (?)
    • (useless in DM-1)

    USE-DM-2

    • SE -NO worries for kidney!
    • -weight gain, hypoglycemia
    • -drug interactions w/ Cimetidine (induce cyps), Salicylates, Sulfonamides
  17. Chlorpropamide
    • first gen Sulfonylurease (secretologue)
    • -close ATP-dep K channel in beta cells--> depol--> Ca influx--> insulin release
    • -decrease glucagon release
    • -increase insulin receptor sensitivity (?)
    • (useless in DM-1)

    USE-DM-2

    • SE- long acting!! watch out in renal disease pt
    • -disulfram-like effects! SIADH!
    • -weight gain, hypoglycemia
    • -drug interactions w/ Cimetidine (induce cyps), Salicylates, Sulfonamides
  18. Glipizide
    • second gen Sulfonylureas
    • -close ATP-dep K channel in beta cells--> depol--> Ca influx--> insulin release
    • -decrease glucagon release
    • -increase insulin receptor sensitivity (?)
    • (useless in DM-1)

    USE-DM-2

    • SE- watch out in liver disease pt
    • -weight gain, hypoglycemia
    • -drug interactions w/ Cimetidine (induce cyps), Salicylates, Sulfonamides
  19. Glyburide
    • second gen Sulfonylureas (secretologue)
    • -close ATP-dep K channel in beta cells--> depol--> Ca influx--> insulin release
    • -decrease glucagon release
    • -increase insulin receptor sensitivity (?)
    • (useless in DM-1)

    USE-DM-2

    • SE- active metabolite! watch out in kidney disease
    • -weight gain, hypoglycemia
    • -drug interactions w/ Cimetidine (induce cyps), Salicylates, Sulfonamides
  20. Glimepiride
    • second gen Sulfonylureas (secretologue)
    • -close ATP-dep K channel in beta cells--> depol--> Ca influx--> insulin release
    • -decrease glucagon release
    • -increase insulin receptor sensitivity (?)
    • (useless in DM-1)

    USE-DM-2

    • SE-weight gain, hypoglycemia
    • -drug interactions w/ Cimetidine (induce cyps), Salicylates, Sulfonamides
  21. Metformin
    • Euglycemic (Biguanides)
    • -decrease postprandial glucose (decr liver glucose!)
    • -does NOT cause hypoglycemia or weight gain!
    • inhibit intracellular enzymes
    • -decrease gluconeogenesis
    • -increase glycolysis
    • -increase glucose uptake by GLUT-4 in SKM (insulin sensitivity)
    • (maybe activate PPAR transcription factors)

    • USE- (oral) monotherapy or combo DM-1, DM-2 can be used in pts w/out islet fxn.
    • -synergistic w/ sulfonylureas!

    • SE- Lactic acidosis!! , GI distress
    • DO NOT use in renal failure!!
  22. Acarbose
    • alpha-glucosidase inhibitor
    • -block intestinal brush-border alpha-glucosidase
    • -decrease glucose absorption-->decrs postprandial glucose-->insulin demand
    • -NO hypoglycemia!

    USE-monotherapy or combo for DM-2

    SE- GI! diarrhea (osmotic), hepatotoxity
  23. Miglitol
    • alpha-glucosidase inhibitor
    • -block intestinal brush-border alpha-glucosidase-decrease glucose absorption-->decrs postprandial glucose-->insulin demand
    • -NO hypoglycemia!

    USE-monotherapy or combo for DM-2

    SE- GI! diarrhea (osmotic), hepatotoxity
  24. Pioglitazone
    • Glitazone/ Thiazolidinedione
    • -insulin sensitizer (like metformin)
    • -bind PPAR-gamma transcription factor (nuclear receptor) for insulin-response genes (bypass insulin-receptor/signaling)--> sensitize to insulin
    • -decrease liver gluconeogenesis
    • -increase insulin receptor #s!
    • -increase HDL

    USE- monotherapy for DM-2 or combo

    • SE- less hypoglycemia than sulfonylurease
    • -weight gain, edema
    • -CV toxicity, hepatotoxicity
    • -bone fractures..
  25. Rosiglitazone (Avandia)
    • Glitazone/ Thiazolidinedione
    • -insulin sensitizer (like metformin)
    • -bind PPAR-gamma transcription factor for insulin-response genes (bypass insulin-receptor/signaling)--> sensitize to insulin
    • -decrease liver gluconeogenesis
    • -increase insulin receptor #s!
    • -increase HDL

    USE- monotherapy for DM-2 or combo

    • SE -less hypoglycemia than sulfonylurease
    • -weight gain, edema
    • -CV toxicity, hepatotoxicity
    • -bone fractures..
  26. Important genes that are altered by PPAR-Y?
    • ultimately decreases resistance to insulin!
    • -increase Adiponectin (cytokine sec by fat cells)
    • -increase FA transport protein
    • -increase Insulin receptor substrate
    • -increase GLUT-4
  27. GLP-1 normal action?
    • released by L-cells in GI in response to food
    • -GPCR--> Gs--> cAMP!
    • induce satiety
    • decrease gastric emptying
    • increase insulin release
    • -very short half life, so GLP-1 meds are analogs
  28. Exenatide
    • GLP-1 (incretin) receptor agonist
    • -normally: eat--> SI-->GLP-1-->pancreas--> increase insulin release, decrease glucagon--> decrease glucose
    • -enhance glucose-dependent insulin secretion

    • USE- (injected) DM-2
    • -decrease appetite!! great for losing weight too.

    SE- nausea, vomiting, hypoglycemia w/sulfonylureas, pancreatitis!
  29. Sitagliptin (Jenuvia)
    • GLP-1 enhancer
    • -block DPP-4 (dipeptidyl peptidase)--> inhibit breakdown of endogenous GLP-1

    USE- DM-2

    SE- not much..
  30. Pramlintide
    • synthetic amylin
    • -slow GI absorption
    • -decrease glucagon
    • -decrease appetite

    • USE- DM-2
    • -decrease appetite!

    SE- hypoglycemia, nausea, diarrhea
  31. treatment for gestational diabetes?
    • Insulin!
    • oral hypoglycemic meds are generally avoided in GDM b/c risk of fetal hyperinsulinemia and hypoglycemia.
  32. Hypoglycemia can occur w/ use of Insulin and Sulfonylurease, unlike Metformin and TZDS..
  33. Modes of action of DM drugs
    Inhibit glucose absorption: Acarbose, Miglitol

    Inhibit glucose production: Metformin, Pioglitazone, Rosiglitazone

    Enhance glucose uptake: Metformine, Pioglitazone, Rosiglitazone

    Increase insulin release: Sulfonylureas, Exenatide, Sitaglipin
  34. Adrenal insufficiency? Adrenal crisis?
    -signs? what do you immediately give?
    vomiting, abdominal pain, weight loss, anorexia, hypotension, hypoglycemia, hyperpigmentation

    Rx-Corticosteroids (stress dose of hydrocortisone)!!
  35. Propylthiouracil
    • thioamide
    • -block thyroid peroxidase
    • -high dose block 5'deiodinase
    • -block organification of iodied and coupling of thyroid hormone synthesis
    • -cross placenta, but highly protein bound, so safer

    USE- hyperthyroidism

    SE- maculopapular rash, aplastic anemia, agranulocytosis (rare)
  36. Methimazole
    • thioamide
    • -block thyroid peroxidase
    • -block organification of iodied and coupling of thyroid hormone synthesis
    • -cross placenta, high free form, so do NOT use in pregnancy. Use Proplthiouracil

    USE- hyperthyroidism

    SE- maculopapular rash, teratogen, aplastic anemia, agranulocytosis (rare)
  37. Propranolol
    • nonselective beta blocker
    • -also blocks 5'deiodinase (block T3-->T3)

    USE-hyperthyroidism

    SE- sedation, bradycardia, AV block, hypotension, bronchospasm, vasospasm.. (look at b-blockers)
  38. Perchlorate/ pertechnetate
    • block Na/Iodide symporter on thryoid follicular cell (basolateral side)
    • -competative inhibition
  39. Iodide (Lugol's solution)
    • KI + I2 (Lugol's solution)
    • -inhibit release of T3 and T4 from Thyroglobulin
    • -decrease thyroid gland size, vascularity

    USE- preOP use in thyrotoxicosis

    SE- no long term use b/c thyroid gland "escapes" from effect afte 2wks..
  40. Drugs that decrease peripheral conversion of T4-->T3?
    • Propylthiouracil
    • Glucocorticoids
    • Amiodarone (hypothyroidism in iodine sufficient regions, thyrotoxicosis in iodine defficient regions)
    • Iopanoic acid
    • Propranolol (non selective beta-blockers)
  41. What do you give to Grave's disease patient with severe Opthalmopathy?
    • Glucocorticoids!
    • -decrease severity of inflammation and decrease extraocular volume.
    • -conventional antithyroid drugs do NOT improve opthalmopahty (edema+ lympthocyte, mac infiltration+ fibroblasts make too much PGs)
  42. Levothyroxine
    • Thyroxine analog
    • replace thyroxine

    USE- hypothyroidism, myxedema

    SE- tachycardia, heat intolerance, tremor, arrhythmia
  43. Triiodothyronine
    • Thyroxine analog
    • replace thyroxine

    USE- hypothyroidism, myxedema

    SE- tachycardia, heat intolerance, tremor, arrhythmia
  44. Growth hormone
    Hypothalamic/pituitary drug

    USE-GH deficiency, Turner syndrome
  45. Somatostatin (Octreotide)
    Hypothalamic/ Pituitary drug

    USE-Acromegaly, Carcinoid syndrome, Gastrinoma, Glucagonoma
  46. Oxytocin
    Hypothalamic/Pituitary drug

    USE- Stimulate labor, uterine contractions, Milk let-down, Uterine hemorrhage.
  47. Desmopressin (ADH)
    ADH analog

    • USE- central diabetes incipidus
    • -Hemophlia A, vWF disease (stimulate endothelial release of vWF + VIII)
    • -Enuresis!
    • -not much effect on V1 receptors so no vasoconstiriction
  48. Demeclocycline
    • ADH antagonist
    • -member of tetracycline

    USE- SIADH (syndrome of inappropriate ADH)

    SE- Nephrogenic diabetes insipidus, Photosensitivity, bone + teeth abnormalities
  49. Hydrocortisone
    Predisone
    Triamcinolone
    Dexamethasone
    Beclomethasone
    • Glucocorticoids!
    • -inhibit PLA2, block expression of COX-2
    • -decrease production of leukotriens and Prostaglandins

    USE-Addison's disease, inflammation, immune suppression, asthma

    • SE- Iatrogenic Cushing's syndrome- buffalo hump, moon facies, truncal obesity, muscle wasting, think skin, easy bruisability, osteoporosis adrenocortical atrophy, peptic ulcers, diabetes ( if chronic)
    • -Adrenal insufficiency if drug is stopped after chronic use!
  50. Leuprolide
    • GnRH analog
    • -agonist properties when used in pusatile fashion
    • -antagonist properties when used continuously.

    • USE- infertility (pusatile)
    • - Prostate cancer (continuous, use w/ Flutamide)
    • -Uterine fibroids, Endometriosis, DUB (continuous)

    SE- Antiandrogen, nausea, vomiting
  51. Testosterone (methyltestosterone)
    Androgen receptor agonist

    • USE- Hypogonadism, pormote development of secondary sex characteristics
    • -stimulate anabolism for recovering burns, injury
    • -treat ER-positive breast cancer (exemestane)

    • SE- masculinization in females, reduce intratesticular testosterone in males (inhibit LH release)--> gonadal atophy
    • -Premature closure of epiphyseal plates
    • -increase LDL, decrease HDL
  52. Testosterone---5-alpha reductase--> DHT (more potent)
  53. Finasteride
    • 5apha-reductase inhibitor
    • -block Testosterone--> DHT

    USE- BPH, hair growth

    to prevent male patterin hair loss, give a drug that'll promote female breast growth
  54. Flutamide
    • testosterone, DTH receptor blocker
    • nonsteroidal, competitive inhibitor of androgens

    USE- Prostate carcinoma
  55. Ketoconazole
    • Inhibit steroid synthesis
    • -block Desmolase

    USE- PCOS (polycystic ovarian syndrome) to prevent Hirsutism

    SE- gynecomastia, amenorrhea
  56. Spironolactone
    • K-sparing diuretic
    • -block Aldosterone receptor
    • -also block other androgen receptors

    USE- PCOS to prevent hirsutism

    SE- gynecomastia, amenorrhea
  57. Estrogens
    -Ethinyl estradiol
    -DES
    -Mestranol
    Estrogen receptor agonists

    • USE-hypogonadism, ovarian failure, mesntrual abnormalities, HRT in postmenopausal women
    • -Men: androgen dependent prostate cancer

    • SE-increase risk for endometrial cancer, bleeding in postmenopausal women
    • -DES exposure in utero--> clear cell carcinoma of vagina
    • -hypercoagulability
    • DO NOT use in ER-positive breast cancer, History of DVT!
  58. Clomiphene
    • SERMs (selective estrogen receptor modulators)
    • Estrogen partial agonists in hypothalamus
    • -prevent normal feedback inhibition
    • -increase release of LH and FSH--> ovulation

    USE- infertility, PCOS

    SE- hot flashses, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances
  59. Tamoxifen
    • Estrogen partial agonists
    • SERM
    • -antagonist on breast tissue -partial agonist in bone, endometrium
    • USE-
  60. Raloxifene
    • Estrogen partial agonist
    • SERM
    • -agonist on bone
    • -reduce bone resorption

    USE- Osteoporosis
  61. HRT- Hormone replacement therapy
    • USE-relief or prevention of menopausal symptoms
    • (hot flashes, vaginal atrophy)
    • -Osteoporosis (increase Estrogen, decrease osteoclast)

    • SE- unopposed estrogen replacement therapy increase risk of endometrial cancer (so add progesterone)
    • -possible increase of CV risk
  62. Anastrozole/ Exemestane
    aromatase inhibitors

    USE- postmenopausal women w/breast cancer
  63. Progestins
    • -progesterone receptor agonist
    • -increase vascularization of endometrium

    • USE- oral contraceptive addjunct
    • - endometrial cancer
    • -abnormal uterine bleeding
  64. Mifepristone
    (RU-486)
    • -competitive inhibitor of Progestins
    • -block progesterone receptor

    • USE- Termination of pregnancy
    • -given w/ Misoprostol (PGE1-analog: PG cause uterine contraction + cervical dilation)

    SE- heavy bleeding, GI effects ( nausea, vomiting, anorexia), abdominal pain (b.c anti-pregestin effects stimulate release of endogenous prostaglandins and sensitize myometrium to effects of hormone)
  65. Oral contraceptives
    • Synthetic progestin+ estrogen
    • -prevent estrogen surge, LH surge does NOT occur--> NO ovulation

    Advantages- reliable, decrease rick of endometrial, ovarian cancer, decrease incidence of ectopic pregnancy, decrease pelvic infections, regulation of meses

    Disadvantages- taken daily, NO protection against STDs, Increase TGs, Depression, weigh gain, nausea, HTN, hypercoagualability

    Do NOT use in smokers>35 y.o (increase CV events), hx of DVT, stroke or hx of estrogent-dependent tumor!!
  66. Dinoprostone
    • PGE2 analog
    • -cause cervical dilaiton, uterine contraction

    USE- induce labor
  67. Ritodrine/ Terbutaline
    • beta-2 agonist
    • -relax urterus

    USE- reduce premature uterine contractions
  68. Tamsulosin
    • alpha-1 blocker
    • -inhibit smooth muscle contraction
    • -selective for alpha-1 A,D receptors in prostate!
    • (vascular- alpha-1 B)

    USE- BPH
  69. Sildenafil
    • block cGMP PDE--> increase cGMP
    • -relax smooth muscle of corpus cavernosum
    • -increase blood flow, penile erection

    USE- erectile dysfunction

    SE-headache, flushing, dyspepsia, impaire blue-green color vision, risk of life-threatening hypotension if on nitrates!!
  70. Vardenafil
    • block cGMP PDE--> increase cGMP
    • -relax smooth muscle of corpus cavernosum
    • -increase blood flow, penile erection

    USE- erectile dysfunction

    SE-headache, flushing, dyspepsia, impaire blue-green color vision, risk of life-threatening hypotension if on nitrates!!

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