Muscarinic antagonists part 2 Flashcards
what are some clinical uses on muscarinic antagonists?
- COPD
- asthma
- Parkinson’s
- overactive bladder
- mydriatics (ophthalmic exams)
- IBS-D (to stop diarrhea)
what are CNS adverse effects of muscarinic antagonists?
confusion, hallucinations, delirium, and possibly a coma
what are peripheral adverse effects of muscarinic antagonists?
dry eyes, constipation, tachycardia, dry skin, decreased urination (DECREASED SLUD)
what are structural features of the structures of the CNS anti-muscarinic drugs?
they all have tertiary nitrogens because the quaternary are always ionized so they will never be able to get through the blood brain barrier
what two drugs are interactions with muscarinic antagonists? why?
benedryl and antitriptaline because they are competitive antagonists for the same receptor
why are muscarinic antagonists used as mydriatic agents?
they paralyze ciliary eye muscle which causes the lens to be incapable of bending to accommodate for light
when should mydriatic agents be avoided in the patient?
if they are already taking other antimuscarinics because it could be too much if they were given one to dilate they’re eye (cycloplegia)
what is the suffix of drugs that do not have CNS effects?
“ium”
what happens when you relax the sphincter muscle of the eye?
it causes dilation
what happens when you relax the ciliary muscle of the eye?
it causes the lens to flatten and the inability to see far
what should you always be aware of when you go to the doctor to get your eyes dilated?
if you’re on any other muscarinic antagonists
Which type of receptor is involved in vestibular nausea?
M1
How can we use the M1 receptor to prevent nausea?
We can use an M1 antagonist to prevent the nausea before it occurs
can muscarinic antagonist treat all forms of OAB?
no, only some forms
How does urination work?
when sufficient urine is in your bladder, your stretch receptors fire which causes the parasympathetic neurons to fire and the motor neurons that are holding the internal sphincter together to relax. Then the smooth muscle contracts and you relax your external sphincter to release the urine when you’re ready.
What structure is present in all of the drugs used in COPD?
they have a quaternary ammonium compound
what structure is present in all of the drugs used in Parkinson’s?
they all have a tertiary ammonium compound that is able to penetrate the CNS
does dicyclomine that is used to treat IBS-D have to potential to cause CNS adverse effects?
yes because it only has a tertiary amine
what is mydriasis?
dilation of the eye
can muscarinic blockers cause mydriasis?
yes
is scopolamine good at treating nausea after it is already onset?
no, it is only a preventative medication
of all the drugs we were given to treat OAB, do they all have the same effectiveness? what makes them different?
relatively, the only thing that changes is the amount of ADRs from use which is due to the amount of times the medication has to be taken. this is because longer-use drugs flatten out the AUC and decrease the probability of reaching toxic levels.
what is good about drugs for OAB that are more specific for M3?
they will not cause bradycardia in the patient by binding the the M2 receptors in the heart
what is functional selectivity?
for some reason when the drug is taken in the human it has more attraction for receptors on a certain tissue than the same receptors on the other and we are not sure why
when do we see functional selectivity in antimuscarinics? what drug?
when M3 antagonists for some reason bind to M3 receptors in the bladder more than M3s in the salivary galnds
-solifenacin
which two drugs would be primarily be affected by 3A4 inhibitors?
solifenacin and darifenacin because they are highly metabolized by 3A4 in the liver
which drug would be most affects by genetic polymorphisms of 2D6?
darifenacin because it is primarily metabolized by 3A4 and 2D6 in the liver
which drug for OAB can you not give to old people and why?
Oxybutynin because it is very very lipophillic and only has a tertiary amine. this means it will very easily get through the blood brain barrier, expecially those of old people because theirs is starting tho wear down. if it gets into their brains it could cause the decreasee of ACh and the increase of dopamine which would cause major issues.
which two drugs for OAB are prodrugs for 5-HMT? are they still pharmacologically active molecules as prodrugs?
fesoterodine and tolterodine.. YES
what side affects would you see in someone that had poor 2D6 metabolism versus overactive 2D6 metabolism in regards to fesoterodine and tolterodine?
because both the active metabolite and the prodrug are active molecules, they will see no difference in effect. however the poor metabolizer would have more prodrug and the good metabolizer would have more metabolite
why is fesoterodine more predictable than tolterodine?
because tolterodine has to be hydroxylated on a methyl group and fesoterodine is activated by taking off an ester and replacing it with an alcohol
since fesoterodine and tolterodine are basically the same, how do we tell which one will have more affect than the other?
by which ever one is less protein bound, that drug will have more effect
