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MODA > PNS pharma > Flashcards

PNS pharma Flashcards

1
Q

Bethanechol

A

`

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2
Q

an irreversible muscarinic antagonist

A

benzylcholine mustard

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3
Q

anticholinesterase- reversible, short-acting/non-covalent

A

edrophonium

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4
Q

anticholinesterase- reversible, medium acting/covalent

A

(carbamates)
physostigmine, rivastigmine= non-charged, crosses BBB
neostigmine, pyridostigmine= charged, stays in periphery

note: the carbamates are transferred to Ser203 of triad on AchE and carbamylated AChE is more stable, takes minutes to hydrolyse

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5
Q

anticholinesterase- irreversible, long acting

A

organophosphgorus molecules, include:

  • insecticides: parathion, malathion
  • nerve gases: sarin, soman, tabun, novichoks
  • previously used drugs (in glaucoma): echothiophate, Dyflos/DFP

note: all are uncharged and interact with catalytic triad ony (except echothiophate)

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6
Q

edrophonium facts

A
  • too short acting to be therapeutically useful
  • charged, can’t cross membrane– can’t reach CNS
  • its earlier use was in diagnosis of MG (myasthenia gravis) –> the facial weakness and ptosis shows improvement within minutes of drug application
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7
Q

antidotes for organophosphorus poisoning

A
  • atropine

- pralidoxime (2-PAM) = reactivates AChE; oxime is a strong nucleophile

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8
Q

antidotes for organophosphorus poisoning

A
  1. atropine:
    - as it is lipid soluble it can counteract the effects systemically
  2. pralidoxime (2-PAM):
    - reactivates AChE; oxime is a strong nucleophile therefore captures the phosphate group and liberates Ser 203
    - doesn’t cross BBB; therefore, can’t be used when CNS is affected
    - used with atropine
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9
Q

current clinical uses of AChE inhibitors

A
  • in treatment of myasthenia gravis: neostigmine, pyridostigmine (both don’t cross BBB)
  • to reverse the actions of non-depolarising blockers at NMJ after surgery: neostigmine
  • to treat mild to moderate dementia in Alzheimer’s: those that cross BBB
  • (previously) as a test for MG- edrophonium (has been largely replaced by antibody testing and electrical conduction studies)
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10
Q

current clinical uses of AChE inhibitors

A
  • in treatment of myasthenia gravis: neostigmine, pyridostigmine (both don’t cross BBB)
  • to reverse the actions of non-depolarising blockers at NMJ after surgery: neostigmine
  • to treat mild to moderate dementia in Alzheimer’s: those that cross BBB
  • (previously) as a test for MG- edrophonium (has been largely replaced by antibody testing and electrical conduction studies)
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11
Q

what are the enzymes involved in the biosynthesis of catecholamines (e.g. adrenaline)

A
  1. TOH (tyrosine hydroxylase) = tyrosine->DOPA
  2. DDC (DOPA decarboxylase) = DOPA->dopamine
  3. DBH (dopamine beta-hydroxylase) = dopamine->Noradrenaline
  4. PNMT = Noradrenaline-> adrenaline
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12
Q

inhibitors of catecholamine synthesis:

1) TOH
2) DDC
3) DBH

A

1) alpha-methytyrosine
2) carbidopa
3) disulfiram

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13
Q

methyldopa

A

False neurotransmitter at noradrenergic synapses

  • taken up into presynaptic termini;
  • converted to alpha-methyl DA by DDC
  • converted to alpha-methyl NA by DBH
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14
Q

inhibitors of catecholamine synthesis:

1) TOH
2) DDC
3) DBH

A

1) alpha-methytyrosine
- competitive inhibitor of TOH; blocks the rate limiting step and therefore is the only effective way to decrease NT production
2) carbidopa
3) disulfiram

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15
Q

methyldopa

A

used as an antihypertensive in cases which are difficult to treat
False neurotransmitter at noradrenergic synapses
-taken up into presynaptic termini;
-converted to alpha-methyl DA by DDC
-converted to alpha-methyl NA by DBH
-alpha-methyl NA is taken into vesicles and released with NA (and in place of some NA)
-alpha-methyl NA is more active on alpha-2 adrenoreceptors compared to alpha-1 receptors

-alpha-methylnoradrenaline results in a drop in blood pressure

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16
Q

inhibitors of catecholamine synthesis:

1) TOH
2) DDC
3) DBH

A

1) alpha-methyltyrosine (was used for pre-op treatment of phaeochromocytoma)
- competitive inhibitor of TOH; blocks the rate limiting step and therefore is the only effective way to decrease NT production

2) carbidopa with L-DOPA (parkinson’s treatment)
- exogenous L-DOPA is taken up by
3) disulfiram

17
Q

methyldopa

A

used as an antihypertensive in cases which are difficult to treat
False neurotransmitter at noradrenergic synapses
-taken up into presynaptic termini;
-converted to alpha-methyl DA by DDC
-converted to alpha-methyl NA by DBH
-alpha-methyl NA is taken into vesicles and released with NA (and in place of some NA)
-alpha-methyl NA is more active on alpha-2 adrenoreceptors compared to alpha-1 receptors

-alpha-methylnoradrenaline results in a drop in blood pressure

18
Q

inhibitors of catecholamine synthesis:

1) TOH
2) DDC
3) DBH

A

1) alpha-methyltyrosine (was used for pre-op treatment of phaeochromocytoma)
- competitive inhibitor of TOH; blocks the rate limiting step and therefore is the only effective way to decrease NT production

2) carbidopa with L-DOPA (parkinson’s treatment)
- exogenous L-DOPA used to boost DA synthesis; L-DOPA is taken up by cell and converted to DA
- normally, L-DOPA is degraded outside the cell by peripheral decarboxylase
- carbidopa can’t cross BBB; it inhibits peripheral decarboxylase so that the L-DOPA isn’t broken down

3) disulfiram
- used in treatment of alcohol addiction; inhibits alcohol dehydrogenase enzyme
- experimentally used to inhibit DBH

19
Q

methyldopa

A

used as an antihypertensive in cases which are difficult to treat
False neurotransmitter at noradrenergic synapses
-taken up into presynaptic termini;
-converted to alpha-methyl DA by DDC
-converted to alpha-methyl NA by DBH
-alpha-methyl NA is taken into vesicles and released with NA (and in place of some NA)
-alpha-methyl NA is more active on alpha-2 adrenoreceptors compared to alpha-1 receptors

-alpha-methylnoradrenaline results in a drop in blood pressure

20
Q

NA vesicular storage

A

-typically clear-cored vesicles
-stored with ATP in ratio 4:1
-
-

21
Q

catecholamine vesicular storage

A
  • NA with ATP in clear-cored vesicles
  • NA stored with ATP in ratio 4:1
  • NA, ATP and NPY- dense-cored vesicles
  • NA and DA loaded by VMAT-2
22
Q

Reserpine

A
  • high affinity, irreversible blocker of VMAT-2
  • binds to amine substrate site of VMAT-2 and blocks uptake of monoamines (DA, NA,5-HT)
  • leads to depletion of stored NA
  • acts in periphery and the brain; used as antihypertensive previously but was discontinued as it causes severe depression
  • recovery from reserpine blockade requires synthesis of new vesicles
23
Q

FDA approved VMAT-2 inhibitors

A
  • tetrabenazine and valbenazine
  • reversibly bind to VMAT-2 and block uptake of catecholamines (mainly DA)
  • used to manage abnormal involuntary movements associated with Huntington’s disease, tardive dyskinesia etc.
24
Q

FDA approved VMAT-2 inhibitors

A
  • tetrabenazine and valbenazine
  • reversibly bind to VMAT-2 and block uptake of catecholamines (mainly DA)
  • used to manage abnormal involuntary movements associated with Huntington’s disease, tardive dyskinesia etc.
25
Q

agent causing direct blockade of adrenergic neurons

A

Guanethidine:

  • uptake into presynaptic adrenergic nerve terminal via NET
  • loaded into vesicles by VMAT-2 ; causes gradual and long lasting depletion of NA
  • in very high doses it can irreversibly damage the nerve
  • was previously used to treat hypertension
26
Q

indirectly acting sympathomimetic

A

dexamphetamine and tyramine
-they are not adrenoreceptor agonists but make good substrates for monoamine transporter; therefore they don’t act on postsynaptic receptor but are taken up y the transporter at presynaptic terminal

  • transported into terminal by NET (& DAT)
  • loaded into vesicles by VMAT-2, therefore displaces NA
  • the displaced NA collects in the presynaptic terminal and some is metabolized by MAO but mostly escapes to the synapse by reverse transport via NET(&DAT) and acts on postsynaptic receptors
27
Q

MAO

A

enzyme that breaks down NA at presynaptic terminal

28
Q

indirectly acting sympathomimetic

A

dexamphetamine and tyramine

  • CNS stimulants: used in narcolepsy; paradoxically in ADHD
  • they are not adrenoreceptor agonists but make good substrates for monoamine transporter; therefore they don’t act on postsynaptic receptor but are taken up y the transporter at presynaptic terminal
  • transported into terminal by NET (& DAT)
  • loaded into vesicles by VMAT-2, therefore displaces NA
  • the displaced NA collects in the presynaptic terminal and some is metabolized by MAO but mostly escapes to the synapse by reverse transport via NET(&DAT) and acts on postsynaptic receptors

MDMA

  • more profound impact on 5-HT release
  • is a hallucinogenic (called ecstacy)
29
Q

MAO

A

enzyme that breaks down NA at presynaptic terminal

30
Q

mixed acting sympathomimetics

A

ephedrine
-can indirectly release NA like the indirectly acting BUT can also directly act on adrenoreceptors

uses:

  • a nasal decongestant; causes NA-mediated vasoconstriction in the nose
  • airway relaxation by acting on bronchial beta-2- adrenoreceptors
31
Q

explain ‘cheese effect’– what class of drugs does it have to do with?

A

-

MODA (2 decks)

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