Random 3Rd Block Pharm Stuff

Front 1

What metabolic effect does estrogen have?

Back 1

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

Front 2

When not bound to estrogens what are estrogen receptors bound to?

Back 2

HSPs

Front 3

What are the 2 different estrogen receptor genes

Back 3

ER-alpha and ER-beta

Front 4

How is ethanyl estradiol bound?

Back 4

serum albumin

Front 5

should women take estrogens if they are pregnant?

Back 5

NO: can cause reproductive tract toxicities

Front 6

What is the relationship between migraines and hormones?

Back 6

HRT can cause severe migraines (especially estrogens)?

Front 7

What are the different types of synthetic estrogens?

Back 7

ethinyl estradiol (OC, HRT)
Mestranol (OC)
DES - can cause clear cell carcinoma of the vagina

Front 8

What effect does tamoxifen have on bone? What is it used for?

Back 8

Anti-resorptive effects on bone
inhibits proilf of breast ca

Front 9

tamoxifen effects on cholesterol??

Back 9

decreases total cholesterol
decreases LDL
decreases lipoproteins
doesn't increase HDL

Front 10

What effects are seen with raloxifene?

Back 10

anti-resorptive effects on bone
anti-prolif effects on some breast CAs

Front 11

what are the agonist/antagonist effects caused by raloxifene?

Back 11

antoagonist effects on endometrium, ER + breast Ca

Front 12

what effects does roloxifine have on cholesterol?

Back 12

Decreases total cholesterol and LDL
no increase in HDL

Front 13

MOA of clomiphene

Back 13

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

Front 14

Use of fulvestrant

Back 14

can treat tamoxifen resistant breast ca

Front 15

What are ethe different types of aromatase inhibitors?

Back 15

Type I (steroidal)
Type II (non-steroidal)

Front 16

How do nonsteroidal aromatase inhibitors work?

Back 16

they interact reversibly with the heme group of aromatase
steroidals irreversibly inactivate aromatase

Front 17

What are the aromatase inhibitors?
What are they used for?

Back 17

exemastane
letrozole
anastrozole
treat breast Ca

Front 18

Benefit of aromatase inhibitors?

Back 18

don't increase risk of uterine cancer or venous thromboembolism
lipid profile alterations unknown

Front 19

What effect do progestins have on neuroendocrine system?

Back 19

Decresae frequency of GnRH pulse from hpothalamus
Increase amplitude of LH from pit

Front 20

What effects does progestin hvae on reproductive tract?

Back 20

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

Front 21

What effects does progeestin have on CNS?

Back 21

incresaes basal body temp at ovulation
increases ventilatory response of resp centers to CO2
Has depressant and ypnotic actions in CNS (give at bedtime)

Front 22

What effect does progestin have on cholesterol?

Back 22

increases LDL
no effeect, r modest reduction in HDL

Front 23

Which hormone affects aldosterone

Back 23

progestin

Front 24

What are the different progesterone receptors and how do they differ?

Back 24

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

Front 25

what does mifepristone do?

Back 25

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

Front 26

Uses of mifepristone

Back 26

induction of labor after fetal death
tx of endometriosis, leiomyomas, br CA, and meningiomas
luteal phase contraceptive

Front 27

What does progestin do during HRT?

Back 27

reduces uterine cancer risk

Front 28

What effect does progestin have on GnRH?

Back 28

Diminishes frequency of GnRH pulse (impt for ovluation)

Front 29

what does estrogen do to FSH?

Back 29

suppresses FSH release from pit during follicular phase

Front 30

How do progestin only pills work?

Back 30

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

Front 31

What does testosterone do to LH?
How much testsosterone is required for sprematoenesis?

Back 31

inhibits LH secretion
100x greater concentration required in testes
testosterone cna therefore be used formale contraception

Front 32

What hormonens can be used to treat hives?

Back 32

stanozolol
danazol
(stimulate hepatic synthesis of antihistamines)

Front 33

What can be used to treat hereditary angioedema?

Back 33

stanozolol
danazol

Front 34

What is the difference between abarelix and leuprolide?

Back 34

abarelix is a GnRH antagonist (treats prostate CA, breast CA, and endometriosis)
leuprolide is a GnRH analog
Both are anti-androgens

Front 35

What do androgen receptor antagonists do to LH and GnRH?

Back 35

increase LH secretion which increases testosterone
used primarily wiht GnRH to treat metastatic prostate Ca

Front 36

Which androgen receptor antagonist has the best safety proflie?

Back 36

bicalutamide
(flutamide = hepatotoxicity, nilutamide = bad side effects)

Front 37

What can flutamide treat in women?

Back 37

hirsutism

Front 38

Where are the different 5-alpha reductase receptors found?

Back 38

I: non genital skin, liver, bone
II: urogenital tissue in men (prostate) and genital skin in men and women

Front 39

MOA of finasteride

Back 39

antagonist of type II 5-alpha reductase

treats BPH (decreases prostate volume and promotes urine flow)

Front 40

MOA of duasteride?

Back 40

antagonist of I and II 5-alpha reductase
treats BPH (decreases prostate volume and promotes urine flow)

Front 41

hydroxycholoroquine

Back 41

treats RA
decreases RF, but doesn't slow dz
requires 3-6 mo to treat

Front 42

leflunomide

Back 42

inhibits pyrimadine synth by inhibiting DHODH which is needed for rUMP production

Front 43

etanercept MOA

Back 43

TNF inhibition through competitive binding of TNF-alpha

Front 44

infliximab MOA

Back 44

TNF inhibition by binding to TNF-alpha

Front 45

adalimumab MOA

Back 45

TNF inhibition

Front 46

anakinra MOA

Back 46

IL-1 antagonist

Front 47

MOA piroxicam

Back 47

COX inhibition

Front 48

MOA meloxicam

Back 48

COX 2 inhibition

Front 49

MOA diclofenac

Back 49

COX inhibitor more potent than indomethacin

Front 50

MOA nabumetone

Back 50

COX 2 inhibition

Front 51

When should estrogens be given to treat osteoporosis?

Back 51

within the first 5 yrs of menopause

Front 52

MOA of estrogen on bones?

Back 52

reduces PTH effects

Front 53

MOA of calcitonin

Back 53

decreases osteoclast fxn to slow bone demineralization

Front 54

what is teriparatide?

Back 54

fragment of PTH

Front 55

MOA of teriparatide?

Back 55

it is different than endogenous PTH... it stimulates new bone formation
(increases number and activity of osteoblasts)

Front 56

adverse effects of teriparatide

Back 56

can cause incresaed incidence of osteosarcoma

Front 57

MOA of bisphosphonates

Back 57

Inhibits osteoclast fxn
stimulates osteoblasts to inhibit osteoclast fxn

Front 58

which bisphosphonate can lead to osteomalacia?

Back 58

etidronate

Front 59

MOA of fluordie

Back 59

stabilizes hydroxyapatite crystals
acts as a mitogen for osteoblasts

Front 60

MOA plicamycin

Back 60

cytotoxic AB to treat PAget's dz
MOA unclear

Front 61

adverse effects of plicamycin

Back 61

sudden thrombocytopenia --> hemorrhage
alters liver and kidney fxn

Front 62

MOA azathioprine

Back 62

purine anti-metabolite
forms thio-GTP that gets incorporated into DNA

Front 63

MOA mycophenolate mofetil

Back 63

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

Front 64

MOA of mTOR inhibitors

Back 64

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)

Front 65

MOA tacrolimus

Back 65

associaes with FKBP12 adn gindsd to calcinuerin to inhibit its activity in T cells

Front 66

What is calcineurin

Back 66

Substrate = NF-AT which translocates from cyotplasm to nucleus when stim by calcineurin and increases transcription of IL2 and other lymphokines

Front 67

MOA daclizumab

Back 67

mAB against activated T cells (not resting T cells)
Competitive antagonism of IL-2 induced cell prolif

Front 68

class of daclizumab

Back 68

anti-cd25 mAB

Front 69

MOA muromonab

Back 69

mAB against CD3 on T cell surfaace
--> T cell depletion from blood and peripheral lymphoid organs
Also reduces fxn of remaining T cells

Front 70

class of muromonab

Back 70

anti CD3 mAB

Front 71

Adverse effects of metformin

Back 71

decreases B12 absorption
severe lactic acidosis

Front 72

contraindications of metformin

Back 72

in states predisposing to tissue anoxia
renal insuff (cleared by kidney)

Front 73

How long does it take for thiozolidinediones to work?

Back 73

weeks-months

Front 74

adverse effects of thiazoladinediones

Back 74

modest weight gain
fluid retention
changes in LDL, HDL, and TGs
anemia
fatal liver damage, check LFTs

Front 75

interactions with thiazoladinediones

Back 75

indeuce enzymes that degrade oral contraceptives (interacts with p450)

Front 76

indications for alpha-glucosidase inhibitors

Back 76

decrease postprandial plasma glucose in type 2 DM
insulin sparing!!!

Front 77

adverse effecdts of alpha-glucosidase inhibitors

Back 77

gas from CHO fermentation in coln
diarrhea
abdominal pain

Front 78

MOA exenatide

Back 78

incretin mimetic (incretins stimulate insulin)
AA sequence similar to human glucagon like peptide !, stimulates insulin secretion, lowers serum glucagon
slows gastric emptying
increases satiety

Front 79

adverse effects of exenatide

Back 79

N/V/D

Front 80

MOA pramlintide

Back 80

slows gastric emptying
increases satiety
suppresses postprandial plasma glucoagon and hepatic glucose output

Front 81

Drawback of glitazone therapy

Back 81

expensive
long-term data lacking

Front 82

which are the most cost effective anti-diabetic agents available?

Back 82

sulfonylureas

Front 83

MOA of sulfonylureas

Back 83

stimulates insulin secretion from beta cells
requires working beta cells (not for DM I)

Front 84

MOA of glitazones

Back 84

reduces insulin resistance by binding to nuclear receptor PPAR-gamma and increases the transcription of genes encoding proteins that mediate insulin action

Front 85

structure of insulin receptor

Back 85

2 alpha subnits that are extracellular and bind insulin
2 beta subunits that are transmembrane and posess tyrosine kinase activity

Front 86

what does insulin binding to receptor lead to

Back 86

glucose transporter translocation to membrane
glycogen synthases activity incresaes
increased lipogenesis
enhanced DNA synthesis and cell growth/division

Front 87

structure of NPH

Back 87

combo of insulin and protamine
nether is present in uncomplexed form

Front 88

structure of lente

Back 88

combo of semilente and ultralente

Front 89

which insulin formulation mimcs basal insulin release from pancreas of non diabetic

Back 89

ultralente

Front 90

what is exubera indicated for

Back 90

DM I and II `

Front 91

what do sulfonylureas do to K channel

Back 91

inhibit efflux of K

Front 92

what is the insulin source (human or animal) for regular?
Lispro?
Aspart?
Glargine

Back 92

human/pork
human
human
human

Front 93

which insulin is available for IV and IV injection pumps?

Back 93

regular

Front 94

which insulin formulation crystallizes into hexamer?

Back 94

glargine

Front 95

benefit of lispro

Back 95

significantly improved glycemic control vs regular insulin, w/o hypoglycemia

Front 96

which insulin prep is associated with low hypoglycemia

Back 96

lispro

Front 97

How does garlic affect clotting?

Back 97

inhibits TX formation and platelet aggregation

Front 98

how does ginkgo affect clotting?

Back 98

inhbits PAF

Front 99

how does feverfew affect clotting?

Back 99

inhibits arachidonic acid synth

Front 100

which type of arsenic is more toxic?

Back 100

inorganic trivalent arsenic (2-10x more toxic than pentavalent)

Front 101

how is inorganic arsenic toxic?

Back 101

binds sulfhydryl groups on proteins

Front 102

what toxicity is associated with arsine gas?

Back 102

massive hemolysis

Front 103

treatment for arsine gas toxicity?

Back 103

chelation ineffective
use exchange transfusion and mannitol

Front 104

which chelator is exremely nephrotoxic?
treats?

Back 104

EDTA
lead poisoning

Front 105

which chelators can be given orally

Back 105

DMPS
succimer
penacillamine