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SIU5 Neurology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Describe the metabolism of AA NT: glutamate.

A
  1. Glutamate (Glu) is an excitatory NT
  2. Glucose and Glutamine (Gln) –> Glu via glutaminase
  3. Glu is stored in the vesicles of the synapse by VGluT- vesicular glutamate transporter
  4. Vesicles are released by Ca dependent exocytosis
  5. Released glu is taken up into nerve cells and glial cells (Astrocytes) by EAAT- excitatory AA transporter
  6. In astrocytes, Glu–> Gln by glutamine synthase, also recycled back to neurone
  7. Gln is recycled via transporters (GlnT) back to neurones
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2
Q

Define nociception

A

Nociception is the physical PROCESS of detection and transmission of damaging (noxious) stimuli

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3
Q

Define nociceptor

A

Structures / receptors which detect noxious stimuli

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4
Q

Define pain

A

Pain is the SUBJECTIVE CONSCIOUS perception of a stimuli that is causing tissue damage

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5
Q

Define Algesia and analgesia

A

Algesia: the induction of a condition leading to nociception and pain
Analgesia: reduction of nociception or pain without loss of conciseness

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6
Q

Describe the metabolism of GABA

A 
TCA cycle gives glutamate 
-> glutamic acid decarboxylase (enzyme) GAD->
GABA!!
- gaba transaminase ->
Succinic semialdehyde (inactive) ->
- succinic dehydrogenase 
Succinate 
- back to TCA cycle
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7
Q

List of inotropic and Metabotropic GABA receptor

describe the characeteristics of two type of rec

A

Ionotropic GABAa : cl- ion channel (hyperpolarise cells- inhibitory)
Metabotropic GABAb: B and Y subunits bind to K/Na channels
Efflux? Inhibitory
GABAc : cl- ion channel (v lil in brain )

inotropic: heterogenous rec, rapid cellular effect
metabotropic: hetero and homodimers, activate 2nd msger system from Gprotein, slower effect, may be “autorec” located Presynaptically

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8
Q

what type of ion channel is GABAa?

How many subunits are within an iontropic GABAa R?

A 
Ligand gated cl- ion channel 
- cl- influx -> IPSP
-fast hyperpol ->inhibition
5 subunits 
2a, 2b, 1 gamma
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9
Q

Where’s the orthosteric and the allosteric site of GABAa R?

A

B/w a and b sites = 2 binding sites within 5 subunits orthosteric (normal GABA binding sites)
B/w a and gamma site = 1 allosteric site (modulator site)

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10
Q

What’s the role of allosteric site of GABAa R

Name some substrates

A

Modulators site ( up and down gating of cl- ions) in presence of GABA bound to orthosteric sites

  • benzodiazepines ag/anta/in. ag
  • channel modulators
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11
Q

What are the functions of GABAa R?

A

1 anaesthetics eg etomidate and propofol
2 barbiturates eg pentobarbital has sedative and anticonvulsant effect
3 benzodiazepines multiple actions eg anxiety relieving, anticonvulsant, hypnotic - go sleepy
4 neurosteroid - Metabolites of progesterone and deoxycorticosterone

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12
Q

GABAb R are …. dimers

What are the roles of the two parts?

A

Heterodimers
R1: fly trap- gaba binding site
R2 traffics the receptor to cell surface

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13
Q

The pharmacological pathway when GABAb R is activated

A

Close ca channel presynaptically reduce NT release - autoreceptor

Open K channel postsynaptically giving a slow hyperpolarisation-inhibtion

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14
Q

The effect of GABAb R agonist
Example
Side effect

A

Treat spasticity : tremour
Motor disorder, multiple sclerosis by inhibiting the descending pathway (ventral root)
Baclofen is an ex
Cross BBB so prob w sedation

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15
Q

What are the three classes of ionotropic glutamate R?

How many subunit does each R has?

A

NMDA -subunit gluN1,N2A-D,N3
AMPA - gluA1-4
KAINATE -glu K1-5
4 subunits = tetrameric

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16
Q

NMDA (ionotropic gluR) is readily blocked by what ion?

How to unblock the R?

A

Mg2+

is Voltage sensitive and disappears when cell is depolarised

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17
Q

What agonists are required for the Activation of NMDA (ionotropic gluR)

A

glutamate on orthosteric site

glycine on allosteric site

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18
Q

What are the selective antagonists of NMDA Rs

A

polyamine ag/antag
Ketamine (sedative)
Phencyclidine (sedative hallucinogenic)

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19
Q

Metabotropic glutamate R has how many different GPCR?

Can be classified into how many groups

A

8 different GPCR : mGluR1-8

3 groups: I,II,III

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20
Q

Characteristics of mGluRs

A

Homo, heterodimers
Slow neuromodulatory role
Connect to diff second messenger system (Gq- increase IP3, Ca) (Gi/ Go reduces cAMP)

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21
Q

NMDA R is highly permeable to which ions

A

ca and Na (excitatory) ->can cause excitotoxicity

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22
Q

What are the effects of presynaptic NMDAR and mGluR

A

NMDAR increase glutamate release by increase Ca influx

mGluR decrease glutamate release by decreasing Ca influx

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23
Q

is amino acid transmitters localised to brain regions?

A

no, they are ubiquitous
glutamate mostly found in pyramidal neurones
GABA mostly found in short local interneurones also in longer projection neurones

24
Q

what is the full name for GABA

A

g-amino butyric acid

25
GABAa rec pharmacology | what type of drug bind to it?
ABBN Anaesthetics- etomidate and propfol (valatile) Barbiturates- pentobarbital (sedative/anticonvulsant) BZS (anxiety/anticonvulsant/hypnotic) Neurosteroid- meabolites of progesterone and deoxycorticosterone
26
How does glutamate bind so many rec?
its is NOT a rigid molecule, diff constituents can rotate along the single bonds, gives diff conformations =9 'rotamers' are possible
27
whare are amine NTs?
``` NADH5: NA Ach DA Histamine 5-HT serotonin ```
28
where are NA and Adr orginated?
NA: locus coeruleus in the brain stem Adr: C1 group
29
where does NA and Adr exert an effect?
diffuse activation of forebrain, particularly cerebral cortex and hippocampus also ascending/ descending pathway
30
what are the effect of amine NTS?
arousal, attention, sleep and survival
31
what are the functions of NA in CNS?
1. brainstem- BP control via baroreceptor reflex 2. descending- movement and pain 3. ascending- arousal and mood, cognitive process eg learning, memory, attention
32
what are the results of depletion/ overactive NA in brain?
depletion of NA in forebrain - depression | overactive NA- mania (bipolar)
33
describe the process of NA synthesis/ then inhibition
1. tyrosine from diet 2. tyrosine->DOPA (tyrosine hydroxylase) 3. DOPA-> dopamine (dopa decarboxylase) 4. dopamine-> NA (DA -b- hydroxylase: only NA neurons express this! occur in vesicles via VMAT- vesicular monoamine transporter) 5. high level of NA swtich off tyrosine hydroxylase- end product inhibtion
34
what are the transporters that involved in reuptake / degradation of NA
NET- norepinephrine transporter MAO/ COMT
35
what effect does cocaine have on NA pathway
block reuptake of NA (block NET and DAT- reward)
36
what effect does ampehtamine have on NA pathway
NA replacement- block NET and DAT-reward
37
Classification of overweight and obesity (adults) BMI
``` healthy 18.5- 24.9 overweight 25-29.9 obesity I 30-34.9 obesity II 35- 39.9 obesity III 40 or more ```
38
Classification of overweight and obesity (adults) waist circumference
men 94- 102 cm high risk, >102 v high risk women 80-88 cm high risk, >88 v high risk 8 cm range for both
39
what is the recommended time per week for moderate intensity physical activity
150 min per week 30min for 5 days
40
Lesion (damage) of the dorsal raphe nuclei (5HT origin) = low 5HT induces ...
HYPER phagia
41
5HT in the periphery is stored in | it generates what signal after feed
enterchromaffin cells in GI mucosa | 5HT is release after food to generate satiety signal
42
how can we increase level of 5HT to REDUCE food intake?
administer precursor tryptophan or 5-hydroxytryptophan (5HTP)
43
which 5HT rec are involved in satiety effect in brain
5HT1B/ 5HT2C (both in arcuate nuclues ARC)/5HT6
44
Leptin therapy in humans only effective in
congenital leptin deficiency NOT Leptin resistant
45
Only anti-obesity drug currently licensed in the UK
orlistat
46
MOA of orlistat
Lipase inhibitor, stop fat from broken down to FA and glycerol, fa wont be absorbed, they stay in gut then come out with faeces
47
s/e of orlistat
“Oily stools” (fats still ingested so..) , abdominal cramps, flatus (gas) with discharge
48
what is Fenfluramine what is the MOA s/e
an analogue of amphetamine w low abuse/addictive potential metabolised to norfenfluramine -->5HT releasing agent + reuptake inhibitor--> more 5HT--> activate 5HT2C rec -->reduce food intake heart valve problem via 5HT2B action
49
does fenfluramine work effectively?
Only produced moderate weight loss, effects temporary
50
what is phentermine why is it w/d? MOA
a releasing agent of NA,DA, 5HT cause pulmonary hypertension due to peripheral NA effect - central action on hypothalamus b2 rec- induce apptite suppresion - increase 5HT, inhibit MAO, increase basal metab rate
51
is A fixed-dose combination of phentermine and the anticonvulsant topiramate better or worse what are the effects of topiramate?
better possible effect on (increase?)mitochondrial carbonic anhydrase metabolism: Mitochondrial CA is known to supply HCO3- for the initial reactions of gluconeogenesis and ureagenesis. also effect on VGSC
52
moa of Bupropion/Naltrexone
bupropion - NDRI, increase NA, DA | naltrexone - opioid antagonist - reduce reward - reduce food intake
53
``` Sibutramine what is it MOA does it work? why w/d ```
sibutramine is a NDRI - increase NA and DA originally an antidepressant - stimulate the POMC, anorexigenic pathway, inhibit AGRP, orexigenic pathway in arcuateARC - increase E expenditure via thermogenesis - short term effect 10%wt loss, but rebounce once stopped = w/d bc increased CVR with high NA
54
what is rimonabant? MOA why is it w/d
a cannabinoid CB1 GPCR INVERSE AGONIST endocannabinoid bind to pre-synaptic CB1, inhibitory response, reduce Ca influx 5HT and DA release. (like weed increase food intake) rimonabant reduce this inhibitory response -w/d due to suicidal thought
55
what drug has similar moa to fenfluramine but better? | what is it and what is its moa
locaserin locaserin is a high affinity 5HT2C rec full agonist and relatively selective for 5HT2B rec (that causes heart valve prob) also stimulate POMC- anorexigenic pathway
56
List the anti obesity meds
1. Olistat 2. Fenfluramine 3. Phentermine (fen-phen) 4. Phentermine + topiramate 5. Bupropion + naltrexone 6. Sibutramine 7. Rimonabant 8. Locaserin

SIU5 Neurology (13 decks)

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