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Pharmacology > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Peptide vs. Steroidal Agents

A

Peptide- cell surface receptor, signal transduction pathway via receptor autophosphorylation/tyrosine kinase cascade, PLC, IP3, DAG, adenylate cyclase, cAMP, PKA, etc

Injected, short half-life, frequent dosages, not orally active

Steroidal- intracellular receptor (cytoplasmic or nuclear), ligand-receptor direct binding to DNA

Very lipophillic

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2
Q

Tissue specific effects of insulin

A

Muscle and adipocyte- stimulation of glucose uptake

Liver and muscle- inhib glycogenolysis, stim glycogen synthesis

Liver- inhib gluconeogenesis

Adipocyte and liver- inhib lipolysis, stim fatty acid synthesis and esterification

Adipose- stim LPL

Liver and adrenals- stim cholesterol synthesis

Hypothalamus- suppresses appetite

All cells- stim amino acid uptake, stim protein synthesis, inhib protein degradation, stim DNA synthesis and cell proliferation, inhib apoptosis

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3
Q

Insulin preparations

A

Short acting synthetic (given with zinc for stability, clear solutions, neutral pH):

lispro- reverses amino acids B28 and B29, decreased hexamer stability

aspart- replacement of B28 proline with aspartic acid, decreased hexamer stability

glulisine- replacement of B29 lysine with glutamic acid, replacement of B3 asparagine with lysine, decreased hexamer stability

Short-acting (given with zinc for stability):

Regular (crystalline)

Intermediate-acting:

NPH (isophane)- protamine (protein that binds insulin) combined with insulin in phosphate buffer, prefered over lente, given as 70% NPH and 30% regular insulin

Lente- precipitate of insulin with increased zinc in acetate buffer. Can’t premix this, so NPH is more preferred

Long-acting:

Ultralente- increased zinc concentrations in acetate buffer. Very variable, has been replaced by glargine and detemir.

Glargine- pH of 4.0, 2 arginine residues added to C terminus of B chain and replace asparagine A21 with glycine to stabilize hexamer formation

Detemir- deleted B30 threonine and attached myristic acid to B29 lysine to stabilize hexamer formation and increases albumin binding

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4
Q

Sulfonylureas

A

MOA- stimulated insulin release via closing ATP sensitive K channels, may also potentiate insulin exocytosis by direct effect on binding proteins in secretory granules

Orally Active

Side effect- hypoglycemia

1st gen- tolbutamide, chlorpropamide (alcohol induced flush, hyponatremia), tolazamide (longer half life so harder to manage blood sugar in elderly)

2nd gen (100x more potent than 1st gen, short half-life)- glyburide, glipizide, glimepiride

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5
Q

Meglitinides

A

Repaglinide and nateglinide

Similar MOA to sulfonylureas in closing K channels

No direct effect on insulin exocytosis

No sulfur in structure (differs from sulfonylureas), so they don’t have problems with allergic responses to sulfur

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6
Q

Metformin

A

Does not cause hypoglycemia bc does not increase insulin, but it does increase the peripheral actions of insulin through AMPK

Decreases hepatic glucose output

Contraindicated with renal impairment, hepatic disease, and history of lactic acidosis (this last one is not a big deal with metformin)

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7
Q

Pioglitazone, rosiglitazone, troglitazone

A

Thiazolidinediones (drug class)

Increases insulin action by increasing glucose transporters

Binds to nuclear receptors PPARgama, regulates gene transcription, especially GLUT4

Troglitazone associated with liver failure, but need to monitor liver function with all of these drugs

Side effects- fluid retention, edema, weight gain, increase risk of heart failure (rosiglitazone and pioglitazone), increase risk of MI and stroke (rosiglitazone), increase risk of bladder cancer (pioglitazone)

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8
Q

Acarbose and miglitol

A

alpha-glucosidase inhibitors

decrease carb absorption

side effects- flatulence, diarrhea, abdominal pain

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9
Q

Colesevelam

A

bile acid binding resin

By weird mechanisms, it also lowers blood glucose

Used for type II diabetes

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10
Q

Exenatide

A

glucagon-like peptide-1 analog (GLP-1)

augments glucose-dependent insulin secretion

given by injection

also liraglutide

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11
Q

Sitagliptin

A

inhibitor of dipeptidyl peptidase-4 (DPP-4), which is the enzyme that degrades incretins like GLP-1

also saxagliptin

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12
Q

Pramlintide

A

synthetic analog of amylin

modulates postprandial glucose levels

suppresses glucagon release

delays gastric emptying

CNS anorectic effects

given as preprandial subQ injection

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13
Q

Drug Interactions

A

Hypoglycemic- ethanol, salicylates, beta-antagonists

Hyperglycemic- epinephrine, beta2-agonists, glucocorticoids, tacrolimus, thiazide diuretics, ca-channel blockers, clonidine, phenytoin, glucagon, diazoxide (can treat hypoglycemic episodes by binding to K channel and keeping it open, decreasing insulin release)

B-agonists main effects are peripherally, not at the pancreas

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14
Q

Vasopressin (ADH)

A

Receptors:

V1- PLC, PI hydrolysis, Ca, PKC, acts on vascular smooth muscle

V2- adenylate cyclase, cAMP, PKA, acts on principal cells and renal collecting duct

Desmopressin is synthetic analog that hits V2 selectively

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15
Q

Desmopressin

A

selective V2 agonist on principal cells in collecting duct

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16
Q

Treatment for Central and Nephrogenic Diabetes Insipidus

A

Central- desmopressin, chlorpropamide (enhances signal transduction), carbamazepine, clofibrate

Nephrogenic- lots of water intake, thiazide diuretics, indomethacin, amiloride (for lithium induced DI)

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17
Q

Treatment for SIADH

A

Water restriction, hypertonic saline

Demeclocycline (intereferes with V2 signal transduction), loop diuretics, lithium (last resort)

Conivaptan and tolvaptan- ADH receptor antagonists

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18
Q

Oxytocin (Pitocin)

A

Stimulates uterine contraction

Stimulates milk ejection from mammary glands

Major use is to induce labor

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19
Q

Other agents that stimulate uterine contraction

A

Can use these to treat post-partum hemorrhage

PG analogs in therapeutic abortion- misoprostol (PGE1 analog), dinoprostone (PGE2 analog)

Ergonovine/methylergonovine

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20
Q

Tocolytic agents

A

These relax uterine smooth muscle to prevent or arrest preterm labor

Beta2 selective agonists- terbutaline, ritodrine: relax smooth muscle

Nifedipine- Ca channel blocker: relax smooth muscle

Indomethacin- PG biosynthesis inhibitor, can also cause pre-mature closure of ductus arteriosus (adverse effect)

Atosiban- oxytocin receptor antagonist

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21
Q

GH agents

A

Somatropin

Mecasermin- recombinant IGF1 with binding protein, given for GH resistance (like in Loron type dwarfism)

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22
Q

LH agent

A

hCG (human chorionic gonadotropin)- acts at LH receptor

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23
Q

FSH agents

A

Menotropins- LH and FSH activity (horse urine)

Urofolitropin- mainly FSH (horse urine)

Follitropin- recombinant FSH

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24
Q

TSH agent

A

Thyrotropin- diagnostic agent used for thyroid cancer to enhance radioactive iodine uptake

Don’t really use for treatment, too expensive and it would be dumb

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25
Q

ACTH agent

A

Cosyntropin- diagnostic use

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26
Q

GHRH Agents

A

All diagnostic agents

Sermorelin- some therapeutic use, hard to mimic the pulsatile release

TRH and CRH

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27
Q

GnRH agents

A

gonadorelin- often given in pulsatile form (IV) to stimulate LH/FSH release, short-acting

Long-acting agents (some LH/FSH stim, but later get suppression):

leuprolide- subcutaneous

histrelin- subcutaneous

nafarelin- nasal spray

goserelin- subcutaneous

triptorelin- IM

ganirelix- GnRH receptor antagonist

cetrorelix- GnRH receptor antagonis

used for adjunct to infertility treatment, treatment of precocious puberty, chemical castration, prostate and breast cancer, endometriosis, and leiyomyomasassss

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28
Q

D2 Receptor agonists

A

Used to treat pituitary adenoma, especially prolactinomas and GH adenomas

Bromocriptine, cabergoline

Used to decrease prolactin secretion, “paradoxical” used to decrease GH release

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29
Q

Somatostatin analogs

A

Used to treat pituitary adenomas

Octreotide, lanreotide

Resistant to enzyme degradation, longer half-life

More selective action, more pituitary and less GI and pancreas

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30
Q

GH receptor antagonist

A

Used to treat pituitary adenoma

Pegvisomant

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31
Q

Thyroid hormones

A

Levothryoxine- T4

Liothyronine- T3

Liotrix- T4 and T3

Use nuclear receptors

Used to treat hypothyroidism, cretinism, suppresses TSH in treatment of thyroid cancer

High doses causes cardiac arrhythmias

Drug interactions- estrogens increase binding of T4 to TBG, glucocorticoids and androgens and salicylates decrease binding of T4 to TBG, propranolol and glucocorticoids and PTU and amiodarone and radiology contrast agents inhibit T4 to T3 conversion

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32
Q

Propylthiouracil

A

Inhibits thyroid hormone synthesis via a few different mechanisms: Inhibits peroxidase oxidation of iodide and inhibits coupling reactions of DIT and MIT. Inhibits peripheral deiodination of T4 to T3 (could make a difference if there is severe thyroid excess, would be better than methimazone in this regard)

75 min half-life (shorter than methimazole)

Can cause agranulocytosis (rare), fever, rash

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33
Q

Methimazole

A

Inhibits peroxidase oxidation of iodide and inhibits coupling reactions of DIT and MIT

Half life of 4-6 hours

Less frequent dosing, easier for patients

Can cause agranulocytosis (rare and would happen early on), fever, rash and obviously, hypothyroidism

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34
Q

Thiocyanate, perchlorate, fluroborate

A

Anti-thyroid drugs (ionic inhibitors)

Interferes with iodide concentration via blocking iodide transporter. compete with Iodide.

These are toxic agents and so not frontline drugs. Can get fatal aplastic anemia with perchlorate

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35
Q

Iodine131

A

Anti-thyroid agent

Acts the same as regular iodine

Used in older patients. Treatment with this often leads to hypothyroidism but it’s easy to bring them back to euthyroidism via thyroid hormones

Used to treat metastatic thyroid carcinoma along with TSH (enhance uptake of radioactive iodine)

Contraindicated in pregnant patients and children

I123 : diagnostic use

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36
Q

Glucocorticoids

A

Like other steroids, lipophilic and well absorbed orally.

Once in cytosol binds to GR (HSP is kicked off) and diffuses to nucleus where transcription occurs.

carbohydrate, protein, lipid “central sparing, peripheral wasting”

Uses: replacement therapy, Congential adrenal hyperplasia (ex: 21 alpha hydroxylase def), inflammatory states, asthma, immunosuppressive (transplant), ulcerative colitis

Overdose will look like a Cushing’s patient. Exogenous cortisol will cause feedback inh on Pituitary will result in decreased ACTH: Adrenals will atrophy

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37
Q

Mineralocorticoids

A

Aldosterone

Increased Na reabsorption in distal nephron/ collecting duct

Increase water absorption, K secretion, H secretion, bicarbonate generation

Fludrocortisone is an aldosterone like drug (125X) with cortisol effects 10X cortisol

38
Q

Adrenocorticosteroids

A

Adverse: adrenal suppression during replacement therapy, fluid and electrolyte abnormalities, edema, hypertension, cataracts, osteoporosis, growth suppression in children

In kidney, cortisol gets converted to cortisone by 11B-HSD so that there are no aldosterone like effects by cortisol binding the MR. Enzyme inhibited by licorice

Oral prednisone gets converted to prednisolone by the liver using 11B-HSD. With liver disease, give prednisolone, don’t mess around.

Prednisone is 4X GR and 0.8 MR.

Triamcinolone, Betamethazone, Dexamethasone are 5X, 25X, 25X more potent on GR, respectively (and 0 on MR) Could be useful in treating someone with congestive heart failure; don’t cause more water retention but could help other problem, like inflammatory state.

Dexamethasone suppression test: If ACTH is suppressed, it is coming from pituitary (Cusing disease state). If not suppressed, look for ectopic source like lung carcinoma.

39
Q

Spironolactone and eplerenone

A

MR (aldosterone) antagonist

Side effects- hyperkalemia, metabolic acidosis, impotence, gynecomastia (androgen effects mainly spironolactone)

Used when there is a state of corisol or aldosterone excess.

40
Q

Mifepristone

A

GR antagonist (not a pure antagonist)

Developed as a progestin receptor antagonist

If treating a female patient at child bearing age, be cautious

41
Q

Mitotane

A

Inhibits biosynthesis of adrenocorticosteroids

Adrenal lytic agent, used to treat inoperable adrenocortical carcinoma.

42
Q

Ketoconazole

A

Inhibits P45017alpha (17,20 lyase) and P450acc (at high doses)

SCC cuts down everything (androgen, cortisol, aldosterone) so it’s a messy approach to bring down adrenocorticoids

anti-androgen

43
Q

Metyrapone and etomidate

A

Anti-adrenocorticoids

Inhibits P45011beta (11-hydroxylase)

44
Q

Estrogens

A

Estradiol- rarely used because it has a very high first pass effect in liver

Ethinyl estradiol- synthetic etrogen with ethinyl substitution at C17, decrease first pass hepatic metabolism, increase oral bioavailability, high potency, used as oral contraceptive

Estrone sulfate- conjugated estrogen, less potent, used in post-menopausal replacement therapy. Worried about breat, ovarian, and uterine cancer with estrogen, so avoid high potency drugs like ethinyl estradiol.

Adverse effects- thromboembolic disease (especially smokers), breast and uterine carcinoma (they are estrogen dependent cancers)

Benefits- decreases pregnancies with associated pathologies, osteoporosis, vasomoter symptoms, cardiovascular disease (HDL up, LDL down), vaginitis, and skin thinning

45
Q

Clomiphene

A

Anti-estrogen

Primary estrogen antagonist effect in pituitary but it’s not very good anywhere else. Pituitary doesnt sense estrogen levels so there is no feedback inhibition; FSH and LH will be increased, which is beneficial for fertility

Main use is to induce ovulation

46
Q

Fulvestrant

A

Anti-estrogen and selective estrogen receptor modifier

Full estrogen receptor antagonist

Used to treat breast cancer with disease progression after tamoxifen therapy

47
Q

Tamoxifen and toremifene

A

Tamoxifen- mixed agonist and antagonist properties, anti-estrogen in breast cancer, estrogenic action on endometrium (negative: due to cancer), estrogenic bone actions (positive: less likely to cause osteoporosis)

Main use is for breast cancer

Toremifene- derivative of tamoxifen. “me too” drug

48
Q

Raloxifene

A

Estrogenic in bone (positive effect)

Anti-estrogen in breast and endometrium (positive effects)

This drug is awesome, so why don’t we use this all the time? The debate is, is it as good as tamoxifen in treating breast cancer? Time will tell.

49
Q

Progesterone derivatives

A

progesterone is not too terribly useful by itself. High first pass metabolism by liver and low oral bioavailability

Hydroxyprogesterone caproate- parenteral use only

Medroxyprogesterone acetate- can be used orally, used in post-meopausal replacement therapy

50
Q

19-nor compounds

A

Progesterone analogs

Don’t have carbon 19 (nor 19)

norethindrone, norgestrel- potent and high oral bioavailability, used in oral contraceptives, androgenic

Adverse: (acne, weight gain, lowers HDL, raises LDL)

norgestimate, desogestrel- less androgenic activity

drospirenone- progestin agonist, spironolactone derivative (MR antagonist)

mifepristone- an anti-progestin, GR antagonist. RU-486 abortion drug with some controversy in this country

51
Q

Mifepristone

A

Anti-progestin, receptor antagonist

for abortions, signals there is no progestin and so there is a signal to menstruate. In the US, not approved for post-coital contraception

52
Q

Oral Contraceptives

A

Estrogen stays the same (usually they build during menstrual cycle) so this is non-physiological

estrogen and progestin combinations- can be monophasic, biphasic, or triphasic, suppresses LH/FSH and ovulation. *don’t be silly and memorize the composition of various oral contraceptives

monophasic is the most non-physiologic. Biphasic has higher dose of progestin for the last 11 days. The first 10 days will have lower progestin so there will be less androgen side effects with biphasic preps. Why not take drug last 7 days? allow menstruation. Triphasic is safer than biphasic because every 7 days progestrone is increased stepwise. Triphasic is most physiologic of all of the preps. More important to take the pill every day!

*Dont let your girl take a triphasic and skip a day of taking the pill

progestin only:

when there is a risk for estrogen related cancers.

norgestrel or norethindrone (mini-pill)

norgestrel (norplant)

MPA (depo-provera) injections that can last months to years for convenience

levonorgestrel (Plan B),

ulipristal (progesterone receptor modulator, suppress LH surge and ovulation)

Progestin only compds increase cervical mucus thickening (sperm barrier), alters endometrium to impain implantation

53
Q

Hormone treatment of breast cancer

A

Selective estrogen receptor modifiers- tamoxifen, toremifene, raloxifene, fulvestrant

Aromatase inhibitors (non-steroidal)- have a nitrogen-containing heterocyclic moiety, binds heme of cyp450, competitive reversible inhibitors of aromatase, anastrozole, letrozole

Aromatast Inhibitors (steroidal)- similar to androgen substrates in structure, suicide inactivators (irreversible), very potent exemestane

54
Q

Trastuzumab

A

Breast cancer treatment

Monoclonal antibody directed against the gene product of HER2/erbB-2/NEU oncogene

Inhibits tyrosine kinase activity (EGF receptor) of oncogene product

30-35% of breast cancers overexpress HER2/erbB-2, associated with highly metastatic, aggressive disease with poor prognostic outlook

cardiovascular side effects

55
Q

Lapatinib

A

Inhibits erbB-1 and erbB-2 tyrosine kinase activity

Binds to internal site on receptor and also inhibits activity of truncated form of the HER2 receptor lacking binding domain

Fairly new so not known if it’s better than trastuzumab or not

Like trastuzumab, used for Non estrogen dependent cancer?

56
Q

Testosterone esters

A

Type of androgen

Esterification makes it more lipid soluble

Testosterone propionate- short acting (2-3 times/week)

Testosterone cypionate- long acting (once every 2-4 weeks)

Testosterone enanthate- long acting (once every 2-4 weeks)

These are what we use, forget the oral androgens

Used to treat- primary hypogonadism and improve nitrogen balance, also treat (rarely though) anemia, osteoporosis, and breast cancer

57
Q

Danazol, fluoxymesterone, methyltestosterone

A

Testosterone that is alkylated at C-17alpha postions, this decreases hepatic metabolism, increases oral bioavailability, but unfortunately they hang out and increases hepatic toxicity.

Oral androgens are rarely prescribed, but body builders still take these via black market.

Used to treat hereditary angioneurotic edema

58
Q

Leuprolide

A

Anti-androgen

Long-acting GnRH analog downregulates receptor in pituitary and less FSH and LH

Treatment in precocious puberty, prostate cancer

59
Q

Ganirelix

A

Anti-androgen

GnRH antagonist

60
Q

Spironolactone

A

Anti-androgen

CYP17 inhibitor

Androgen receptor antagonist, used to treat hirsutism (lots of hair where it shouldn’t be…ie bearded lady) in women

61
Q

Finasteride and dutasteride

A

Anti-androgen

5alpha-reductase inhibitory (finasteride mainly Type II, and dutasteride Types I and II), decreases dihydrotestosterone action

Used to treat BPH adn male pattern baldness

62
Q

Androgen receptor antagonists

A

Flutamide, bicalutamide, nilutamide

Increased LH and FSH due to less feedback inhibition, and increased testosterone levels (not desireable), so use GnRH analog in addition to negate this effect.

Prostate cancer Rx

Bicalutamide has less adverse effects

63
Q

Drugs that inhibit sexual function

A

Anti-hypertensives (diuretics, beta-blockers, Ca channel blockers, vasodilators, alpha 2 agonists),

psychiatric drugs (dopamine antagonists) with increased prolactin levels

anti depressants (anti-cholinergic)

alcohol, nicotine, digoxin, cimetidine, spironolactone, endocrine drugs

64
Q

Drugs that increase sexual function

A

Pentoxifylline- “fluidize” RBCs, improve blood flow

Yohimbine- alpha 2 receptor antagonist

Sildenafil, tadalafil, vardenafil- cGMP phosphodiesterase inhibitor. color vision side effects

Phentolamine- alpha receptor antagonist. Improves blood flow to tissues. Orthostatic hypotension

Apomorphine- dopamine agonist

Alprostadil- prostaglandin E1, intraurethral app, intracavernosal injection

65
Q

Metronidazole

A

Treatment of STDs

Active against anaerobic protozoal parasites

Treats T. Vaginalis

Growing resistance to this

66
Q

Quinolones

A

Treatment of STDs

ciprofloxacin, levofloxacin, ofloxacin

Treatment for chlamydia, gonorrhea

Contraindicated in pregnancy

67
Q

Penicillin

A

Treatment of STDs

Treats syphilis and sensitive gonococcal strains, although most gonococcal are penicillin resistant nowadays

68
Q

Ceftriaxone

A

Treatment of STDs

3rd gen cephalosporin

Therapy of choice for gonorrhea

69
Q

Doxycycline

A

Treatment of STDs

Treats chlamydia, but not recommended for gonococcal infections

Safe for patients with renal impairment because it’s not renally eliminated

Not recommended in pregnancy

70
Q

Azithromycin

A

Treatment of STDs

Treatment of chlamydial infections and nongonococcal urethritis

1 time dose treatment

71
Q

Acyclovir, valcyclovir, famciclovir

A

Treatment of STDs

Treats HSV type 2

*for pharm this phase, just know what drug used to treat which bug. He’s not concerned with the other details

72
Q

Foscarnet and ganiclovir

A

Treatment of STDs

Treats CMV infection

73
Q

Vit D analogs

A

ergocalciferol- D2, Cholecalciferol- D3 require 25-hydroxylation in liver

calcifediol- (25-OH -cholecalciferol), requires 1-hydroxylation in kidney: use if there is just a liver problem

calcitriol (1,25-dihydroxycholecalciferol): if kidney problems use this drug

74
Q

Calcitonin

A

Salmon form is more potent, has direct effect on osteoclast to decrease bone resorption, decrease calcium and phosphate reabsorption in kidney

Used when there are hyperactive osteoclasts

75
Q

Estrogens/Selective estrogen receptor modifier (SERM) effect on bone

A

Acts on osteoblasts to decrease osteoclast recruitment and activation

Estrogens cause synthesis of OPG which is a decoy receptor for ODF (rank ligand). Less rank ligand will interact with the rank receptor on osteoclast and so less osteoclasts will be activated. Beneficial in osteoporosis by decreasing bone resorption

Androgens can be converted to estrogens by aromatase so treating osteoporosis with androgen is maybe useful

76
Q

PTH, Teriparatide

A

intermittent administration promotes bone growth, often combinde with alendronate

Estrogens, calcitonin decrease bone loss; PTH actually causes bone deposition

77
Q

Glucocorticoids affect on Ca, VitD, etc

A

antagonize vit D stimulated intestinal calcium absorption, stimulate renal calcium excretion, block bone collagen synthesis, increase PTH stimulated bone resportion

Negative effect in terms of osteoporosis

78
Q

Denosumab

A

Human monoclonal antibody against RANKL

Mimics effect of OPG

New again, awaiting results

woman has osteoporosis but has risk for breast cancer (BRCA1/2) and so how do you treat her? Denosumab obviously

79
Q

Other non-hormonal agents that act on Ca, bone mineralization, etc

A

Ca supplements: calcium chloride, calcium carbonate (oral)

Thiazide diuretics- reduce renal Ca excretion, useful to inhibit renal Ca stone formation

Fluoride- accumulates in bone and teeth, may stabilize hydroxyapatite, increases bone volume, may increase osteoblast activity, toxicities limit use. No good systemic way to administer

80
Q

Cinacalcet

A

calcium sensor mimetic, enhances sensitivity of parathyroid gland to free ionized Ca to suppress PTH

81
Q

Plicamycin

A

Cytotoxic antibiotic that also decreases plasma clacium concentrations by inhibitin bone resporption

82
Q

Oral Sodium Phosphate

A

binds cree ionized Ca

high risk procedures

83
Q

Edetate disodium (EDTA)

A

Ca chelator

high risk procedures

84
Q

Bisphosphonates

A

Decrease osteoclast function/ decrease bone resorption

Resembles pyrophosphate. Osteoclast eats it and apoptosis ensues

etidronate, pamidronate, alendronate, risedronate, tiludronate, zoledronate, ibandronate

retard formation and dissolution of hydroxyapatite, decreases osteoclast function

etidronate and tiludronate- metabolized into ATP analot and accumulates in osteoclasts which impairs cell function and viability, induces apoptosis, no gastric irritation with etidronate

alendronate- inhibit protein prenylation which is important for osteoclast function, less side effect of decrease bone mineralization

all have gastric irritation except etidronate

zoledronate has some renal toxicity

85
Q

Treatment of osteoporosis

A

Estrogens (front line), bisphosphonates, Vit D analogs, calcitonin, Ca supplements, thiazides

86
Q

Treatment of hypercalcemia

A

Bisphosphonates, calcitonin, plicamycin, gallium nitrate, phosphates, glucocorticoids

87
Q

Treatment of hypocalcemia

A

Vit D analogs, calcium supplements

88
Q

Treatment of hypoparathyroidism

A

Vit D analog

89
Q

Treatment of hyperparathyroidism

A

Cinacalcet

90
Q

Iodide

A

Wolf Chaicoff effect: give exogenous Iodide from sources like amiodarone, Lugol’s soluthion, radiology contrast agents. Iodide is toxic to cell and there is a shut down in T4 and T3 synthesis.

Quick effect to make someone euthyroid before surgery. Also for thyrotoxic crisis (thyroid storm)

Thyroid escape: downregulate Na/I receptors and so high levels of Iodide will no longer inhibit thyroid hormone production (after about 10 days of experiencing wolff-chaikoff effect). So long term treatment choice would be PTU or methimazole

Pharmacology (12 decks)

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