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Course 662 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

Where are biogenic amines present?

A

CNS and PNS

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2
Q

how do drugs affect biogenic amines?

A

drugs will affect synthesis, receptor binding, or catabolism

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3
Q

What is the most common type of psychopharmacology?

A

see slide

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4
Q

Describe the synthesis of catecholamines (for dopamine, norepinepherine)

A

see slide

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5
Q

what are the 2 enzymes that can break down dopamine?

A
  1. monoamine oxidase

2. catechol-o-methy transferase

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6
Q

Norepinepherine is important for

A

sleep and wakefulness, attention, feeding behaviour (and cary also said pain perception)

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7
Q

norepinephrine is important in which nervous system?

A

CNS and ANS -> important in the symapthetic component of ANS

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8
Q

Why is important to consider which aspect of the nervous system a neurotransmitter affects?

A

if they are nonspecific (affect multiple NS) you need to consider the implication for all aspects e.g. for norepinephine affects sympathic so important to consider how it might affect blood pressure, heart rate etc

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9
Q

what are the enzymes that break down norepinephine?

A

see slides

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10
Q

Note

A

we’re not gonna be talking about epinephrine much (dont really understand its affects on CNS and it would have a lot of side effects because it’s treated as a hormone so affecting it would affect a lot of systems)

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11
Q

What is hisamine associated with?

A

arousal and attention in the CNS

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12
Q

what is histamine packed by?

A

VMAT

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13
Q

How is histamine removed from the synapse?

A

no transporter identified

instead broke down by enzyme (methyltransferase)

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14
Q

What receptor subtypes are there for hisamine?

A

all subtypes are metabotropic

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15
Q

What is a precursor for seratonin?

A

typotophan

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16
Q

What is a precursor for seratonin?

A

trypotophan

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17
Q

what is responsible for packaging seratonin?

A

VMAT

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18
Q

How is setatonin removef from the synapse?

A
  1. termindation by reuptake by SERT

2. SEE SLIDE FOR OTHER ONE

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19
Q

what can seratonin not be broken down by?

A

COMT

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20
Q

What metabolite do you get when norepinepherine is broken down?

***repeat for other NT

A

VMA, MHPG

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21
Q

What metabolite do you get when dopamine is broken down?

A

HVA

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22
Q

What metabolite do you get when seratonin is broken down?

A

5-HIAA

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23
Q

why is it important to know that seratonin only has one enzym that breaks it down?

A

because if you block both mechanisms for MOA enzym -> can get seratonin syndrome (see lecture and book)

24
Q

note

A

cary said we don’t need to memorize all the brain areas at this point but we will need to learn about certain pathways later one - he wants us to understand why these pathways are important though

25
Q

what is the most common excitatory neurotransmitter?

A

glutamate

26
Q

what % of the synapses in the CNS release glutanate?

A

~50%

27
Q

how is glutamate synthesized?

A

an enzime called glutamine synthetase is present in glial cells which conver to glutamine, then glutamine is transported???

28
Q

Describe the glutamate glutamine cycle

A

See slides/book

29
Q

what are nonessnetial amino acids versus essnetial ones?

A

ee

30
Q

what are the subtypes of glutamte receptors?

A
  1. NMDA - ion gated
  2. AMPA/kainate - ion gated
  3. mGluR - metabotropic glutamate receptor
31
Q

what are AMPA/kaintate receptors responsible for?

A

the most rapid excitatory post synamptic potential (responsible for majority… see slides)

32
Q

too much glutamate ca be _____? what disorder is this linked to

A

neurotoxic

linked to bipolar disorder

33
Q

why is it important to know the difference between types of glutamate receptiors

A

see lecture

34
Q

what is the main inhibitory neurotransmitter in the CNS

A

GABA

35
Q

How is GABA synthesized

A

precurser is glutamate converted by glutamic acid decarboxylase

requires pyridoxol phosphate derived from vitamin B6

36
Q

What happens if infants have a B6 definiciency in utero

A

seizures - too much excitatory

37
Q

describe the termination of action for GABA

A

see slides

something to do with mitochondria organelles

38
Q

what happens if we inhibit GABA breakdown

A

increase in intracellular levels and an increase in inhibitory action
-> GABA aminotransferase inhibition with sodium dipropylacetate is used as an anticonvulsant (see slide for spelling)

39
Q

what are the types of receptors for GABA

A
  1. GABA-A - ligand gated ion channel

2. GABA-B - metabotropic receptors

40
Q

Why is GABA inhibitory

A

because it’s associated channels are permeable to chloride which has a hyperpolarizing effect on the cell

41
Q

what are the factors that impact the absorption of a drug through the GI tract?

A
  1. rate of dissolution of drug
  2. plasma membrane

**SEE SLIDES

42
Q

what are the factors that impact the absorption of a drug through the GI tract?

A
  1. rate of dissolution of drug
  2. plasma membrane

**SEE SLIDES

43
Q

what is pKa - acid dissociation constant

A

pKa is a property of the drug, and it’s pH at which 50% of the substance is ionized and 50% non-ionized

important to determine drug absorption

44
Q

what is pKa - acid dissociation constant

A

pKa is a property of the drug, and it’s pH at which 50% of the substance is ionized and 50% non-ionized

important to determine drug absorption

45
Q

what pKa values are best absorbed by the GI tract?

A

around 7

46
Q

what pKa values are best absorbed by the GI tract?

A

below 7

47
Q

If a medication is ionized, what happens at the lipid bilayer?

What is it’s non ionized?

A

if it’s ionized/charged it will be repelled

if it’s non-ionized -> it will pass through

48
Q

he wants us to understand the match between the pKa value and the pH of the environment and how the absorption is affected by this (if most of the drug is ionized then there will be very little absorption)

A

see next card for how it affects absorption

49
Q

what is ion trapping?

A

See slide
+ when the drug goes from the GI system into the blood, the blood is much less acidic than the stomach, so the drugs become ionized and they don’t get reabsorbed into the stomach and can get transported where they need to be

50
Q

what is ion trapping?

*note see slide for the 75% thing not sure I get it

A

See slide
+ when the drug goes from the GI system into the blood, the blood is much less acidic than the stomach, so the drugs become ionized and they don’t get reabsorbed into the stomach and can get transported where they need to be (applies to moelcules whose pKa is below 7)

51
Q

the blood supply curculates through the body how often?

A

once per minute

52
Q

what is plasma protein binding and why is it important

A

medications in the blood will bind to certain proteins in the blood, which keeps them from being active. this prevents the drug from acting at it’s target site.

53
Q

what is ‘first-pass’ metabolism?

See slides for more clear explanation

A

Our body deactivates molecules through enzymes in the GI tract and bt cellular senymes in the liver

The direct link between blood flow from the GI system to the liver where many molecules (up to 60%) are metabolized before they can be distribution to the body and brain (known as hepatic first pass)

54
Q

what does the liver do to a drug?

A

makes it less and less lipid soluable and more and more qater soluable so they are easier to excrete

55
Q

what is the enterohepatic circulation?

A

this is a direct link from blood supply leaving the stomach and upper intestines to the liver

56
Q

Is first pass metabolism always bad?

A

no, sometimes it’s even required to have an active drug (like in the case of prodrug)

57
Q

what are Cytochrome P450 Enzymes?

A

a family of isozymes

most important for the metablolism of drugs

Course 662 (10 decks)

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