Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

105 Cards in this Set

  • Front
  • Back
What metabolic effect does estrogen have?
Increases HDL
Increases TGs
Increases clotting factors
Decreases LDL, total cholesterol
might increase galstone formation from incresaed cholesterol in bile and decreasd bile acid secretion
When not bound to estrogens what are estrogen receptors bound to?
What are the 2 different estrogen receptor genes
ER-alpha and ER-beta
How is ethanyl estradiol bound?
serum albumin
should women take estrogens if they are pregnant?
NO: can cause reproductive tract toxicities
What is the relationship between migraines and hormones?
HRT can cause severe migraines (especially estrogens)?
What are the different types of synthetic estrogens?
ethinyl estradiol (OC, HRT)
Mestranol (OC)
DES - can cause clear cell carcinoma of the vagina
What effect does tamoxifen have on bone? What is it used for?
Anti-resorptive effects on bone
inhibits proilf of breast ca
tamoxifen effects on cholesterol??
decreases total cholesterol
decreases LDL
decreases lipoproteins
doesn't increase HDL
What effects are seen with raloxifene?
anti-resorptive effects on bone
anti-prolif effects on some breast CAs
what are the agonist/antagonist effects caused by raloxifene?
antoagonist effects on endometrium, ER + breast Ca
what effects does roloxifine have on cholesterol?
Decreases total cholesterol and LDL
no increase in HDL
MOA of clomiphene
blocks E2 mediated negative feedback on pit, increasing LDH and FSH secretion --> enlarged ovaries and stim of ovaries
increases amp of LH and FSH w/o changing pulse frequency
Use of fulvestrant
can treat tamoxifen resistant breast ca
What are ethe different types of aromatase inhibitors?
Type I (steroidal)
Type II (non-steroidal)
How do nonsteroidal aromatase inhibitors work?
they interact reversibly with the heme group of aromatase
steroidals irreversibly inactivate aromatase
What are the aromatase inhibitors?
What are they used for?
treat breast Ca
Benefit of aromatase inhibitors?
don't increase risk of uterine cancer or venous thromboembolism
lipid profile alterations unknown
What effect do progestins have on neuroendocrine system?
Decresae frequency of GnRH pulse from hpothalamus
Increase amplitude of LH from pit
What effects does progestin hvae on reproductive tract?
promotes secretory endometrium
decreases secretion by endocervical glands, afecting penetration of cervix by sperm
suppresses menstruation and uterine contractility
decresaes rate of premature labor in high risk moms
What effects does progeestin have on CNS?
incresaes basal body temp at ovulation
increases ventilatory response of resp centers to CO2
Has depressant and ypnotic actions in CNS (give at bedtime)
What effect does progestin have on cholesterol?
increases LDL
no effeect, r modest reduction in HDL
Which hormone affects aldosterone
What are the different progesterone receptors and how do they differ?
PR-A and PR-B
They are regulated by estrogen

PR-A inhibits PR-B, causes ovulation and implantation
PR-B has stimulatory actions, responsible for mammary gland development
what does mifepristone do?
antagonises PR, GC receptor and androgen receptor
(also has some progesterone agonist ability)
Blocks PRs in uterus --> decidual breakdown --> detachment of blastocyst --> decreases hCG production --> decreased progesterone secretion from corpus luteum --> further accentates decidual breakdown --> increases uterine PG levels --> expulsion of blastocyst
Uses of mifepristone
induction of labor after fetal death
tx of endometriosis, leiomyomas, br CA, and meningiomas
luteal phase contraceptive
What does progestin do during HRT?
reduces uterine cancer risk
What effect does progestin have on GnRH?
Diminishes frequency of GnRH pulse (impt for ovluation)
what does estrogen do to FSH?
suppresses FSH release from pit during follicular phase
How do progestin only pills work?
block ovulation in 60-80% of cycles
They diminish GnRH frequency and LH surge
Also thicken cervical mucus,which decreases sprem penetration
alters endometrium so implantation is impaired
What does testosterone do to LH?
How much testsosterone is required for sprematoenesis?
inhibits LH secretion
100x greater concentration required in testes
testosterone cna therefore be used formale contraception
What hormonens can be used to treat hives?
(stimulate hepatic synthesis of antihistamines)
What can be used to treat hereditary angioedema?
What is the difference between abarelix and leuprolide?
abarelix is a GnRH antagonist (treats prostate CA, breast CA, and endometriosis)
leuprolide is a GnRH analog
Both are anti-androgens
What do androgen receptor antagonists do to LH and GnRH?
increase LH secretion which increases testosterone
used primarily wiht GnRH to treat metastatic prostate Ca
Which androgen receptor antagonist has the best safety proflie?
(flutamide = hepatotoxicity, nilutamide = bad side effects)
What can flutamide treat in women?
Where are the different 5-alpha reductase receptors found?
I: non genital skin, liver, bone
II: urogenital tissue in men (prostate) and genital skin in men and women
MOA of finasteride
antagonist of type II 5-alpha reductase

treats BPH (decreases prostate volume and promotes urine flow)
MOA of duasteride?
antagonist of I and II 5-alpha reductase
treats BPH (decreases prostate volume and promotes urine flow)
treats RA
decreases RF, but doesn't slow dz
requires 3-6 mo to treat
inhibits pyrimadine synth by inhibiting DHODH which is needed for rUMP production
etanercept MOA
TNF inhibition through competitive binding of TNF-alpha
infliximab MOA
TNF inhibition by binding to TNF-alpha
adalimumab MOA
TNF inhibition
anakinra MOA
IL-1 antagonist
MOA piroxicam
COX inhibition
MOA meloxicam
COX 2 inhibition
MOA diclofenac
COX inhibitor more potent than indomethacin
MOA nabumetone
COX 2 inhibition
When should estrogens be given to treat osteoporosis?
within the first 5 yrs of menopause
MOA of estrogen on bones?
reduces PTH effects
MOA of calcitonin
decreases osteoclast fxn to slow bone demineralization
what is teriparatide?
fragment of PTH
MOA of teriparatide?
it is different than endogenous PTH... it stimulates new bone formation
(increases number and activity of osteoblasts)
adverse effects of teriparatide
can cause incresaed incidence of osteosarcoma
MOA of bisphosphonates
Inhibits osteoclast fxn
stimulates osteoblasts to inhibit osteoclast fxn
which bisphosphonate can lead to osteomalacia?
MOA of fluordie
stabilizes hydroxyapatite crystals
acts as a mitogen for osteoblasts
MOA plicamycin
cytotoxic AB to treat PAget's dz
MOA unclear
adverse effects of plicamycin
sudden thrombocytopenia --> hemorrhage
alters liver and kidney fxn
MOA azathioprine
purine anti-metabolite
forms thio-GTP that gets incorporated into DNA
MOA mycophenolate mofetil
it is a form of mycophenolic acid, which inhibits monophosphate dehydrogenase (needed for do novo synthesis of purines)
B and T cells need this pathway to proliferate
process is inhibited
MOA of mTOR inhibitors
inhibits B and T cell proliferation stimulated by IL-2
Forms complex with FKBP12 that inhibits mTOR activity (mTOR = protein kinase that causes growht and expansion of T and B cells in response to IL-2)
MOA tacrolimus
associaes with FKBP12 adn gindsd to calcinuerin to inhibit its activity in T cells
What is calcineurin
Substrate = NF-AT which translocates from cyotplasm to nucleus when stim by calcineurin and increases transcription of IL2 and other lymphokines
MOA daclizumab
mAB against activated T cells (not resting T cells)
Competitive antagonism of IL-2 induced cell prolif
class of daclizumab
anti-cd25 mAB
MOA muromonab
mAB against CD3 on T cell surfaace
--> T cell depletion from blood and peripheral lymphoid organs
Also reduces fxn of remaining T cells
class of muromonab
anti CD3 mAB
Adverse effects of metformin
decreases B12 absorption
severe lactic acidosis
contraindications of metformin
in states predisposing to tissue anoxia
renal insuff (cleared by kidney)
How long does it take for thiozolidinediones to work?
adverse effects of thiazoladinediones
modest weight gain
fluid retention
changes in LDL, HDL, and TGs
fatal liver damage, check LFTs
interactions with thiazoladinediones
indeuce enzymes that degrade oral contraceptives (interacts with p450)
indications for alpha-glucosidase inhibitors
decrease postprandial plasma glucose in type 2 DM
insulin sparing!!!
adverse effecdts of alpha-glucosidase inhibitors
gas from CHO fermentation in coln
abdominal pain
MOA exenatide
incretin mimetic (incretins stimulate insulin)
AA sequence similar to human glucagon like peptide !, stimulates insulin secretion, lowers serum glucagon
slows gastric emptying
increases satiety
adverse effects of exenatide
MOA pramlintide
slows gastric emptying
increases satiety
suppresses postprandial plasma glucoagon and hepatic glucose output
Drawback of glitazone therapy
long-term data lacking
which are the most cost effective anti-diabetic agents available?
MOA of sulfonylureas
stimulates insulin secretion from beta cells
requires working beta cells (not for DM I)
MOA of glitazones
reduces insulin resistance by binding to nuclear receptor PPAR-gamma and increases the transcription of genes encoding proteins that mediate insulin action
structure of insulin receptor
2 alpha subnits that are extracellular and bind insulin
2 beta subunits that are transmembrane and posess tyrosine kinase activity
what does insulin binding to receptor lead to
glucose transporter translocation to membrane
glycogen synthases activity incresaes
increased lipogenesis
enhanced DNA synthesis and cell growth/division
structure of NPH
combo of insulin and protamine
nether is present in uncomplexed form
structure of lente
combo of semilente and ultralente
which insulin formulation mimcs basal insulin release from pancreas of non diabetic
what is exubera indicated for
DM I and II `
what do sulfonylureas do to K channel
inhibit efflux of K
what is the insulin source (human or animal) for regular?
which insulin is available for IV and IV injection pumps?
which insulin formulation crystallizes into hexamer?
benefit of lispro
significantly improved glycemic control vs regular insulin, w/o hypoglycemia
which insulin prep is associated with low hypoglycemia
How does garlic affect clotting?
inhibits TX formation and platelet aggregation
how does ginkgo affect clotting?
inhbits PAF
how does feverfew affect clotting?
inhibits arachidonic acid synth
which type of arsenic is more toxic?
inorganic trivalent arsenic (2-10x more toxic than pentavalent)
how is inorganic arsenic toxic?
binds sulfhydryl groups on proteins
what toxicity is associated with arsine gas?
massive hemolysis
treatment for arsine gas toxicity?
chelation ineffective
use exchange transfusion and mannitol
which chelator is exremely nephrotoxic?
lead poisoning
which chelators can be given orally