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Therapeutics > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

what are the two types of cholinergic receptors

A

Nicotinic, Muscarinic

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2
Q

Most used cholinergic receptor in drug manipulation

A

Muscarinic

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3
Q

Which nicotinic and muscarinic receptors are used in therapeutic targeting

A

Nm, Nn & M1, M2, M3

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4
Q

What is a cholinergic agent

A

Parasympathetic mechanism involving ACh receptors

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5
Q

What does a direct agonist do in para sympathomimetic mechanism

A

activates cholinoreceptors

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6
Q

what does an indirect agonist do in a parasympathomimetic mechanism

A

Stimulate ACh release or inhibit ACHe

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7
Q

Many drugs exhibit ______ side effects

A

Anticholinergic

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8
Q

does acetylcholine have a higher affinity for nicotinic or muscarinic receptors`

A

muscarinic

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9
Q

What kind of tissue is M1 located in

A

Post ganglionic

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10
Q

M2 tissue location

A

Heart

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11
Q

M3 tissue location

A

Smooth muscle, exocrine glands, endothelium

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12
Q

M4 and M5 tissue location

A

CNS

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13
Q

mnemonic to remember GPCR mechanism of muscarinic receptors

A

QIQIQ

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14
Q

Mnemonic to remember GPCR mechanism of Adrenergic receptors

A

A1- Q
A2- I
B1,2,3- S
QISS

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15
Q

Gq pathway mevhanism

A

DAG—->IP3 and PLC and Ca2+

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16
Q

Gi mechanism of GPCR

A

Inhibition of adenylyl cyclase, K+ channel activation

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17
Q

WHich muscarinic receptor opposes B1 receptor in heart

A

M2

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18
Q

Most common muscarinic receptor

A

M3

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19
Q

Where is M3 found in the body

A

Smooth muscle, exocrine and endothelium

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20
Q

6 steps of ACh synthesis

A

1 choline transported into presynaptic nerve terminal by sodium dependent choline transporter (inhibited by Hemicholium)

2 ACh is synthesized from choline +acetyl CoA by enzyme choline acetyl transferase

3 ACh transported into storage vesicle by second carrier (VAT) (inhibited by vesamicol)

4 ACh binds to cholinoreceptors on post synaptic cell

5 Terminated by ACHe

6 Autoreceptors and receptors on pre synaptic nerve inhibit via Feedback mechanism

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21
Q

Acetylcholine structure

A

COOH-CH2-CH2-N+-(CH3)3

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22
Q

methacholine vs acetylcholine

A

CH3 added to BETA carbon in methacholine

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23
Q

Acetylcholine vs Carbacol

A

COOH replaced by COON

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24
Q

Bethanechol vs Acetylcholine

A

Beta carbon added and H2N added

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25
Q

Why is the methyl on B carbon in methacholine

A

Increases muscarinic binding and decreases nicotinic binding

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26
Q

PSNS symptoms of muscarinic agonist poisoning and why

A

Bradychardia, M2 decreases HR
Diarrhea and cramps, M3 contracts Walls
Bronchoconstriction, M2 and M3 lead to bronchoconstriction
salivation- M3 increases secretion
Visual disturbances- M3 in eye

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27
Q

SNS symptoms of muscarinic agonist poisoning and why

A

Sweating- a1 secretes sweat
Hypotension- uninnervated muscarinic receptors in blood vessel mediating vasodilation via Norepinephrine

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28
Q

Muscarinic agonist effect on heart

A

decrease in HR, conduction and force due to M2 activation

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29
Q

Muscarinic agonist effect on exocrine glands

A

Increases in secretion (Lachrymal, Tracheobronchial, salivary, digestive, sweat glands) sue to M3 activation

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30
Q

Muscarinic agonist effect on smooth muscle

A

M3 increases contraction while M2 inhibits relaxation

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31
Q

Muscarinic agonist effect on sphincters

A

M3 relaxation

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32
Q

stereoisomeric preference of cholinergic receptors

A

Only (+) sterochemistry binds well

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33
Q

How does pilocarpine treat glaucoma

A

M3 agonist leads to contraction of ciliary muscle

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34
Q

Why are antimuscarinic drugs contraindicated in glaucoma

A

M3 will be targeted by antimuscarinic drugs, we need M3 to contract ciliary muscle

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35
Q

When ACh is modified to carbachol what changes

A

ACHe sensitivity decreases, both still used for miosis in surgery and glaucoma

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36
Q

ACHe modified to pilocarpine ACHe sensitivity and change in use

A

Not sensitive, used in glaucoma

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37
Q

ACHe modified to bethanechol ACHE sensitivity and change in use

A

No ACHe sensitivity and is used for urinary retention and post op ileus

38
Q

ACH and carbachol receptors

39
Q

Bethanechol and pilocarpine receptors

40
Q

varenicline

41
Q

clinical use of pilocarpine

A

Glaucoma and dry mouth

42
Q

Clinical use of bethanechol

A

GI stimulation or treatment of urinary retention

43
Q

methacholine clinical use

A

Test for hyperactive airways

44
Q

Carbachol clinical use

A

Ocular (surgery/glaucoma)

45
Q

Varenicline (chantix) use

A

Smoking cessation

46
Q

PSNS side effects Mnemonic

A

DUMBBELSS

Diarrhea, urination, miosis, Bronchoconstriction, bradycardia, Emesis, Lacrimation, salivation, sweating

47
Q

mechanism of varenicline

A

Neuronal nicotinic partial agonist that blocks nicotine binding

48
Q

Indirect acting ACHe inhibitor 3 examples (reversible)

A

Physostigamine, neostigamine, edrophonium

49
Q

Irreversibe ACHe inhibitor

A

Organophosphate

50
Q

Difference between the mechaism of direct vs indirect cholinergic agonist

A

Indirect do not bind to the receptor. They act as ACHe inhibitors, indirectly affecting the amount of ACh in the system. Direct agonists bind and act as muscarinic receptor agonists

51
Q

Types of cholinesterases

A

Plasma cholinesterase and acetylcholinesterase

52
Q

Difference between acetylcholinesterase and plasmacholinesterase

A

ACHe is located in synapse and it is selective to ACh. Plasma cholinesterase is located in the plasma and it is selective for ACh, SUX and procaine

53
Q

Highest turnover rate of any enzyme

54
Q

How is ACh hydrolyzed by ACHe

A

Esteric site in ACHe has serine that binds ester group on ACh and the anionic site binds the positive nitrogen. This breaks the bond.

55
Q

How is ACHe reactivated after splitting ACh.

A

Water reactivates the enzyme

56
Q

Use of the amino acids in esteric and anionic sites in catalysis

A

Lower activation energy needed to proceed with the reaction. Speed up the process.

57
Q

Contrast the structures and molecular interactions of edrophonium with acetylcholinesterase

A

Edrophonium has a positive quaternary nitrogen and and OH group on the ring. Bind to anionic site and block ACh binding. Blocking ACHe activity

58
Q

Is edrophonium reversible or irreversible? Covalent or non-covalent?

A

Reversible non-covalent

59
Q

Contrast the structures and molecular interactions of stigamines with acetylcholinesterase

A

Carbamates that covalently modify AChE and are more SLOWLY hydrolyzed than ACh

60
Q

Are carbamates reversible or irreversible? Covalent or non-covalent?

A

Reversible, covalent

61
Q

What are stigamines

A

Substrates that are more slowly hydrolyzed than ACh. Do not cross BBB

62
Q

Clinical use of edrophonium

A

Myasthenia gravis (MG) (very short acting drug)

63
Q

Clinical use of pyridostigamine

A

Treatment of MG
Reversal of non-depolarizing neuromuscular blockade
Pretreatment for potential nerve gas exposure

64
Q

How is pyridostigmine treatment for nerve gas exposure

A

Occupies ACHE so nerve gas has nowhere to go.

65
Q

Clinical use of Neostigimine

A

Used for MG
reversal of non-depolarizing neuromuscular blockade
Post -op urinary retention

66
Q

The only ACHe inhibitor that can cross the BB is

A

Physostigmine

67
Q

physostigmine clinical use

A

Antidote to anti-muscarinic poisoning

68
Q

Are organophosphates reversible or irreversible? Covalent or non-covalent

A

irreversible, covalent

69
Q

What are the uses of organophosphates

A

For glaucoma

70
Q

What are the organophosphates used in insectiside

A

Malathion and Diazinon

71
Q

Why are malathion and diazinon rapidly inactivated in mammals

A

Insects have CYt P450 which metabolize p=5 to p=0, which is extremely toxic. mammals lack Cyt p 450

72
Q

mechanism of organophosphates on ACHe

A

Organophosphates do not bind anionic site, the bind directly to esteric site and they form a covalent bond

73
Q

Why is organophosphate to toxic

A

The phosphate covalent bond is extremely stable so it can not be hydrolyzed by water like normal. Water can not reverse hydrolyze it.

74
Q

What is ageing in organophosphates

A

Ageing happens when a functional group on the organophosphate leaves and forms a negative phosphate. Once ageing happens it can not be detoxified.

75
Q

What can we use to treat organophosphates before ageing happens?

A

Pralidoxime (2-PAM)

76
Q

Does pralidoxime cross the BBB?

77
Q

Since pralidoxime does not cross the BBB, what can we use along with it to treat organophospahte poisoning

78
Q

Atropine can not block________ receptors

79
Q

Why can alzheimers be cured by cholinesterase inhibitors

A

Alzheimers is loss of cholinergic neurons in brain. So it can be treated with cholinesterase inhibitors

80
Q

How does donepezil slow progression of alzheimers? does it slow the progression of the disease?

A

Bind to anionic site and block ACh binding. NO it does not slow progressions only enhances cognitive ability

81
Q

Donepezil reversible or irreversible? covalent or non-covalent?

A

reversible and non-covalent

82
Q

How does rivastigamine (exelon) enhance cognitive ability in alzheimers

A

By increasing cholinergic function

83
Q

How does Galantamine prevent alzheimers

A

it is a competitive AChE inhibitor

84
Q

Which drug is an NMDA receptor antagonist to treat alzheimers

85
Q

What are NMDA receptors

A

NMDA receptors are found in the CNS where they are activated by glutamate in areas associated with cognition and memory

86
Q

Why do glutamate regulators improve memory, attention, reason and language in alzheimers pateints

A

Neuronal loss in alzheimers may be related to increased activity of glutamate

87
Q

Which two drugs are approved for moderate to severe alzheimers

A

Donepezil and memantine

88
Q

physostigmine clinical use

A

Treats anticholinergic poisoning, glaucoma and alzheimers

89
Q

organophosphate example. What does it treat

A

Echothiophosphate, treats glaucoma

90
Q

parasympathomimetic side effects

A

DUMBBELSS
(diarrhea, urination, miosis, bronchoconstriction, bradycardia, emesis, lacrimation, salivation, sweating

91
Q

treatment for cholinergic agent side effects and toxicity

A

cholinergic receptor antagonist (atropine)

92
Q

Treatment for cholinergic agent side effects if irreversible

A

2-PAM (pralidoxime)

Therapeutics (46 decks)

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