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Uni year 1 > Drugs > Flashcards

Drugs Flashcards

1
Q

What are agonists?

A

Agonists are drugs that bind to a receptor to produce a response. They have affinity and efficacy.

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2
Q

What is the efficacy of a full agonist?

A

1

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3
Q

What is an antagonist?

A

A drug that binds to a receptor but does not produce a response. They have affinity but not efficacy.

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4
Q

What is the equation for occupancy?

A

p = [AR]/[Rt] = [A]/Kd + [A]

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5
Q

Where are benzodiasepine receptors found and what are they?

A

They are allosteric modulatory sites on GABAA receptors increasing the affinity for GABA and increasing channel opening

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6
Q

What are the different types of antagonism

A 
competitive antagonists
irreversible antagonists
allosteric antagonist 
channel blockers
physiological antagonists
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7
Q

What is an example of a physiological antagonist?

A

acetylcholine and adrenaline in the heart, they produce opposite effects on the tissue and produce a non-selective suppression of the response

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8
Q

What are local anaesthetics?

A

reversibly block nerve conduction when applied to a restricted area of the body without loss of consciousness.
All local anaesthetics contain a benzene ring

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9
Q

How do local anaesthetics work?

A

Sodium channels blocked so AP can’t be generated to send information from nociceptors to brain

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10
Q

What is an example of a local anaesthetic?

A

lidocaine (medium length)

bupivacaine (long length)

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11
Q

What factors can affect the effectiveness of local anaesthetics?

A

tissue pH
- infection can lead to increased acidity which can lead to an increased in ionised form making it less effective
sensitivity of nerve fibres
- smaller diameters (eg nociceptor neurones) are more sensitive so are more affected by LAs

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12
Q

What does drug absorption depend on?

A
  • route of administration
  • chemical nature eg lipohilic, charge, size
  • packaging
  • blood flow rate to site of delivery
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13
Q

What is the volume of distribution?

A

How much drug needs to be in the body to get a certain concentration in the plasma
Vd = total amount of drug in body/amount of drug in plasma

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14
Q

What are cytochrome P450s?

A

Used in phase 1 metabolism of drugs, can metabolise a wide range of different molecules, creates highly reactive compounds as substrates for phase 2

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15
Q

What molecules could be used for conjugation in phase 2 metabolism?

A

glutathione
sulfate
glycine
glucaronic acid

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16
Q

Paracetamol metabolism

A

phase 1 - N-hydroxylation by CYP2E1 or CYP1A2 to form NAP2D6

phase 2 - conjugation to glutathione

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17
Q

What are the routes for excretion?

A

Renal - filtration and secretion
Hepatic/biliary - faecal
sweat, breath

18
Q

What are the receptors at the neuromuscular junction?

A

nicotinic acetylcholine receptors

19
Q

What transports acetylcholine into vesicles and what blocks it?

A

An ACh carrier

Vesamicol

20
Q

What the choline transporter (to the plasma membrane)?

A

hemicholinium

21
Q

What blocks exocytosis of the vesicle of ACh?

A

toxins

22
Q

What are types of neuromuscular blockers?

A

non-depolarising blockers - antagonists - tubocurarine

depolarising blockers - agonists - suxamethonium

23
Q

How do non-polarising blockers work?

A

They are competitive antagonists at nACHRs

They decrease the endplate potential so not enough receptors are occupied by ACh

24
Q

How do polarising blockers work?

A

Suxamethonium is an agonist at nAChRs and cause endplate depolarisation. Action potentials cause fasciculations. It isn’t broken down by acetylcholinesterase so it causes prolonged depolarisation

25
Q

What can be used to treat myasthenia gravis and how does it work?

A

Cholinesterase inhibitors can be used to increase ACh levels to overcome decrease in nAChRs
eg edrophonium, neostigmine

26
Q

How is noradrenaline and adrenaline synthesised?

A
  1. Tyrosine is converted to DOPA by tyrosine hydroxylase
  2. DOPA is converted to dopamine by DOPA decarboxylase
  3. Dopamine is converted to noradrenaline by dopamine-beta-hydroxylase
  4. noradrenaline is converted to adrenaline by phenylethanolamine N-methyl transferase
27
Q

What is the rate limiting step in NAd/Ad synthesis?

A

tyrosine to DOPA

28
Q

What is tyrosin hydroxylase inhibited by?

A

a-methyltyrosine

29
Q

What is DOPA decarboxylase inhibited by?

A

carbidopa

30
Q

What is dopamine-beta-hydroxylase inhibited by?

A

nepicastat and etamicasta

31
Q

Where are noradrenaline and adrenaline stored?

A

In vesicles, chromaffin granules

32
Q

What can inhibit noradrenaline release?

A
  • acetylcholine via muscarinic receptors
  • adenosine inhibits release via exocytosis
  • opioids via muscarinic receptors
33
Q

What facilitates noradrenaline release?

A

Angiotensin II via AT1 receptor

34
Q

What inhibits noradrenaline uptake?

A

Noradrenaline transporter inhibitors enhance sympathetic activity
desiprimine - tricyclic antidepressant

35
Q

What are the enzymes involved in degradation of catecholamines?

A
  • monoamine axidases which are bound to surface of mitochondria and convert catecholamines to aldehydes
  • Catechol-O-methyl transferases which converts catecholamines to methoxy derivatives
  • aldehyde dehydrogenase
    aldehyde reductase
36
Q

Where is acetylcholine made, what is it made from and what catayses it?

A

Pre-synaptic terminal
acetyl and choline
choline acetyltransferase

37
Q

What is an example of an agonist for the benzodiazepine receptor?

A

Diazepam

38
Q

What is an example of an antagonist for the benzodiazepine receptor?

A

flumazenil

39
Q

What is an example of an inverse agonist for the benzodiazepine receptor?

A

betacarbolines

40
Q

What is myesthenia gravis?

A

A disease due to failure at the NMJ
Muscle weakness during sustained activity
Autoimmune
Lack of nAChR

41
Q

What are the uses of cholinesterase inhibitors?

A

Reverse effects of non-depolarising NMJ blockers - increase ACh levels to compete with antagonist and cause EPP

Treat myasthenia gravis by increasing ACh levels to overcome decrease in nAChRs

Uni year 1 (19 decks)

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