Med Chem, Adrenergic Neurotransmission

Front 1

how many NE bound to ATP

what form is this

Back 1

4

storage form

drugs will disrupt this

Front 2

methyltyrosine inhibits tyrosine hydroxylase and has been used in the tx of ----

Back 2

pheochromocytoma

Front 3

methyrosine inhibits --- by binding to substrate active site

Back 3

tyrosine hydroylase

Front 4

metyrosine reduces ---, thereby reducing -----

Back 4

NE

BP

Front 5

this med is a substrate for dopa decarboxylase and decrases bp

Back 5

methyldopa

works centrally and peripherally

Front 6

carbidopa inhibits --- -----

this will prevent conversion of l dopa to ----

Back 6

dopa decarboxylase

dopamine

Front 7

which med will compette w/ ne to bidn to ATP

used as antiHTN

Back 7

guanethidine

basic pka= 12

doesn't cross bbb

polar: why will compete w/ NE to bind w/ ATP

NE will be depleted by MAO. . . it's no longer in vesicles. . . exposed

Front 8

how does reserpine get into brain

Back 8

ph= 7

so 1/2 can get into brain

Front 9

why isn't reserpine used

Back 9

depeletes ne centrally and peripherally

Front 10

bretyllium inhibit release of ne from ---------

due its -- --- structue it can't xbbb

Back 10

nerve terminal

quaternary ammonium

Front 11

bretyllium blocks entry of --- and prevent NE from being released

Back 11

Ca

Front 12

Bretyllium prevents -- absorption

used for htn crisis the --- route

used in cardiac ----- . . . slow herat rate

Back 12

oral

IV

arrythmias

Front 13

which isomer of xopenex is active

Back 13

R

Front 14

se of albuterol

Back 14

ha

anxiety

blurred vision

Front 15

no ch3 on the r2 position for sudafed pe will lead to what

Back 15

metabolization by cyp450 and mao

Front 16

why ar amphetamines lipophilic

Back 16

no OH groups

Front 17

what does amphetamine do in the hypothalamus

Back 17

incease NE

drug of abuse and speed

Front 18

amphetamine prevents/reverses uptake of --- and ----

Back 18

NE

DA

Front 19

which is more lipophilic amphetamine or methamphetamine

Back 19

methamphetamine

Front 20

why's sudafed not effective

Back 20

has a 3-oh, so it's polar and can't xbbb

metabolized quickly by mao

Front 21

key features of alpha 2 agonist

Back 21

dicholoro

heteroa

atom: O, N, S

open chain imidazoline

Front 22

pka of imidazoline around

Back 22

8 so can cross bbb

decrease bp

Front 23

t/f

imidazoline are acidic

Back 23

f

basic

protonated at physiological pH: don't absorb well. . . so use topically

can cause rebound constriction

Front 24

phentolamine is alpha 1 and 2 antag

why is this bad

Back 24

want to block alpha 1, but not alpha 2

Front 25

acitve isomer of bb

Back 25

s

but fools receptor to think it's R, which is ne

Front 26

which are more cleared by the liver:

lipophilic or hydrophilic

Back 26

lipophilic

Front 27

hydrophillic compounds are cleared by the

Back 27

kidney

Front 28

R1 on b adrenergic antag is polar then

Back 28

if polar then B1 selectivity

Front 29

R2 on the b adrenergic antag means. ..

Back 29

ISA activity

Front 30

if beta adrenergic antag is para ( across) to the oxypropanol group then

Back 30

B1 selective

Front 31

if beta adrenergeric antag is ortho (next to) oxypropanonol group then?

Back 31

isa activity

Front 32

which do you need more of atropine or scopolamin

Back 32

atropine

cuz diluted w/ R isomer

Front 33

uses of atropine and scopolamine

Back 33

diarrhea

incontinence

used ot cause mydriasis

cough/cold prep: decrease secretions

motion sickness

decrease GI propulsion

Front 34

se of atropine and scopolamine

Back 34

stop tears

Front 35

polar para on labetol signifies what

Back 35

more selective for B1 than B2

Front 36

labetalol has isa activity

Back 36

t

although no othro

Front 37

synthetic subs for atropine/scopolamine include

Back 37

quaternary: robinol

Front 38

synthetic subs for atropine/scopolamine include

Back 38

agents used in opthhal

homatropine

cyclopentolate

tropicanide

Front 39

synthetic subs for atropine/scopolamine include

Back 39

agents used for obstructive pulmonary disease

ipratropium

oxitropium

Front 40

robinal uses

Back 40

decrease lung secretions

urinary incontinence

Front 41

two drugs that's nonspecific and used for urinary incontinence

Back 41

tolterodine

oxybutynin

Front 42

3 classes of ACh-ase inhibitors

Back 42

competitve inhibitors

mechanistic-based inhibitors

semi-reversible inhibitors

Front 43

competitive inhibitors of Ach recognize --- --- --- binding pocket of achase

Back 43

aromatic amino acid

Front 44

two competitive inhibitors of ach

Back 44

donepezil

tacrine

Front 45

mechanistic based inhbitors of ach recognize --- --- binding pocket of achase and go thr same hydrolysis rxn as Ach, but, the rxn is much slower

Back 45

serine protease

Front 46

two mechanistic based inhibitors of ach

Back 46

physostigme

rivastigmine

Front 47

semi-reversible inhibitors inhibit enzyme by forming ---- esters of the serine residue in the acitve site and then being slowly ----- reducing the amount of free Ache that can hydrolyze Ach

Back 47

carbamyl esters

hydrolyzed

Front 48

meds of semi-reversible inhbitiors

Back 48

physostigmine

neostigmine bromide

pyridostigmine bromide

Front 49

physiostigme binds to ache to form a ---- ---- which then is hydrolyzed slowly makeing the free enzyme unavailabe

Back 49

carbamylated enzyme

Front 50

physostigme binds to the --- site of the enzyme

Back 50

anionic

this decreasee the potency as a fx of the pH

Front 51

what does neostigmine bromide tx

Back 51

myastenia gravis

reverse skeletal muscle paralysis caused by curare

stimulate urinary tract

Front 52

how does neostigmine br work

Back 52

similar to physostigmine and

direct stimulation of cholinegic receptors

Front 53

pyridostigmine bromide is used in chronic management of

Back 53

myasthenia gravis

Front 54

which semi-reversible inhibotor is better tolerated

Back 54

pyridostigmine br

Front 55

mechanistic based semi reversible inhibitors recognize --- ---- pocket of achase and go thru same hydrolysis rxn as ach but hte rxn is much ----

Back 55

serine protease

slower

Front 56

pka of rivastgimine

Back 56

9

enoug to xbbb

Front 57

t1/2 of rivastigmine

Back 57

1.5 hr

after 5 hrs 60% still inhibiting Ach

dose BID

Front 58

se of rivastigmine

Back 58

insomnia

decreased chronotrophic

decreased inotrophic

decreased perfusion

gi: slud

Front 59

which is used as prophylaxis for nerve gas

Back 59

pyridostimine bromide

gulf war syndrome

Front 60

most irreverislbe achase inhibitors

Back 60

organophosphorus

Front 61

mechanism of irreversible inhbition involves the formation of a phosphorylated serine residue int he --- site of Ache

Back 61

esteric

Front 62

mechanism of irreversible inhbition formation of the --- --- requires activation of hte serine residue as in the formation of the of the --- ----- intermediate

Back 62

phospyoryl ester

acetyl-enzyme

Front 63

how is the irrevesible different from the semi-reversible (rivastigme)

Back 63

they hydrolysis rxn is unsuccessful

Front 64

t/f

nerve gases are not gases

Back 64

t

Front 65

ex of nerve gases

Back 65

sarin

VX

Front 66

2pam is an antidote for --- ----

Back 66

organophosphate poisoning

Front 67

what's a better nucleophile

2 pam or water

Back 67

2pam

Front 68

what's hard to hydrolyze on sarin

Back 68

the F group