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eLCRS - 팜 > ANXIOLYTICS, SEDATIVES AND HYPNOTICS > Flashcards

ANXIOLYTICS, SEDATIVES AND HYPNOTICS Flashcards

1
Q

Describe CENTRAL GABA-MEDIATED INHIBITION

A
  • short axon GABA interneurones in the brain –> has regulatory role
  • keep firing rates within certain parameters
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2
Q

Glutamate = precursor for GAB
GLU –> converted to GABA (via GAD)
- GABA = stored in vesicle in presynaptic terminal
-

A

-

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3
Q

Describe the synthesis of GABA

A 
Glutamate = precursor for GAB 
GLU --> converted to GABA (via GAD)
- GABA = stored in vesicle in presynaptic terminal 
- until depolarization occurs 
- VGCC opens 
- Causes exocytosis
  • chloride flows into post synaptic cell –> causes hyperpolarisation
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4
Q

Describe the metabolism of GABA

A
  1. GABA = converted to –> Succinic semialdehyde (SSDH)
    - via GABA- Transaminase
  2. SSDH = converted to –> Succinic Acid
    - via succinic semialdehyde dehydrogenase

Succinic Acid - goes back o TCA Cycle

NOTE:
GABA-T + SSDH = Mitochondrial enzymes
- Inhibitors of GABA Metabolism leads to large accumulation of Brain GABA

Anticonvulsive drugs:

  • SODIUM VALPROATE (EPILIM)
  • -> SSDH + GABA T inhibitor
  • VIGABATRIN (SABRIL)
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5
Q

Describe the reuptake of GABA

A
  • primary inactivation method of GABA
  • uptake into glial cells / presynaptic cells
  • GABA –> converted to SSA (Via GABA-T)
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6
Q

describe the structure of the GABAa receptor complex

A
  • GABA receptor protein
  • Barbiturate receptor protein
  • BDZ receptor protein
  • chloride channel protein

GABAA receptor complex: (post-synaptic) 4 main proteins (not inc. modulin)

  • GABA binds GABA receptor protein à links w/ BDZ receptor protein mediated by GABA modulin à opens Cl- channel proteins
  • If BDZ binds BDZ receptor protein à enhances GABA action on Cl- channel

o Also, binding/affinity of GABA is enhanced

o This is reciprocal: binding of GABA enhances affinity of BDZ too

  • BARB enhances GABA action at Cl- channel + GABA affinity (not reciprocal)

o At high doses, BARBs directly stimulate Cl- channel

  • Triangle = Bicuculline is competitive GABAA receptor antagonist
  • Rectangle = Flumazenil is competitive BDZ antagonist
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7
Q

how do Bz + Barbs similar / differ

A

SIMILARITY:
- No activity alone b/c work by enhancing GABA (allosteric action

DIFFERENCE:

  • -> Different binding sites + mechanisms:
  • BZs increase frequency of openings (same duration)
  • BARBs increase duration of openings (no frequency change)

–> BARBs = less selective than BZs
o Cause decreased excitatory transmission
o Other membrane effects e.g. at high doses

o May explain why:

  • BARBs can induce surgical anaesthesia (BZs can’t do this)
  • BARBS have low margin of safety
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8
Q

What are some clinical uses of BZs + BARBS ?

A

ANAESTHETICS (BARBs ONLY : THIOPENTONE)

ANTICONVULSANTS (DIAZEPAM; CLONAZEPAM; PHENOBARBITAL)

ANTI-SPASTICS (DIAZEPAM)

ANXIOLYTICS

SEDATIVES / HYPNOTICS

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9
Q

define anxiolytics

A

anxiolytics : REMOVE ANXIETY WITHOUT IMPAIRING MENTAL OR PHYSICAL ACTIVITY

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10
Q

Define sedatives

A

SEDATIVES: REDUCE MENTAL AND PHYSICAL ACITVITY WITHOUT PRODUCING LOSS OF CONSCIOUSNESS

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11
Q

Define Hypnotics

A

HYPNOTICS: INDUCE SLEEP

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12
Q

BZ + BARBS clinically

IDEALLY: THEY SHOULD:

i) HAVE wide / narrow MARGIN OF SAFETY
ii) depress / not depress RESPIRATION
iii) produce/ do not produce NATURAL SLEEP (HYPNOTICS)
iv) interacts / doest interact WITH OTHER DRUGS
v) produces / doesn’t produce ‘HANGOVERS’
vi) produces / doesn’t produce DEPENDENCE

A
  • IDEALLY: THEY SHOULD:
    i) HAVE WIDE MARGIN OF SAFETY
    ii) NOT DEPRESS RESPIRATION
    iii) PRODUCE NATURAL SLEEP (HYPNOTICS)
    iv) NOT INTERACT WITH OTHER DRUGS
    v) NOT PRODUCE ‘HANGOVERS’
    vi) NOT PRODUCE DEPENDENCE
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13
Q

What are clinical uses of barbiturates?

what is half life of barbiturates

A
  • sedative / hypnotic
  • -> Amobarbital
  • -> severe intractable insomnia
  • -> Half life = 20 - 25hrs
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14
Q

What are unwanted effects of barbiturates?

A
  • DEPRESS RESPIRATION
  • OVERDOSING = LETHAL
  • alters natural sleep (decreases REM) –> Hangovers / Irritability
  • potentiates effects of other CNS Depressants e.g alcohol
  • enzyme inducers
  • tolerance development
  • withdrawal syndrome (insomnia, anxiety, tremor, convulsions, death)
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15
Q

Describe the pharmacokinetics of Benzodiazepines

A
  • PEAK [PLASMA] ~ 1h
  • binds to plasma proteins strongly
  • highly lipid soluble
  • metabolized extensively in liver
  • excreted via urine (glucuronide conjugates)
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16
Q

Benzodiazepines –> ALL act at GABAa receptors

A

-

17
Q

What are the 2 types of

A

SHORT-ACTING
e.g temazepam, oxazepam

LONG-ACTING
–> tends to have slower METABOLISM
+ ACTIVE METABOLITES
e.g diazepam , nor diazepam

18
Q

Longer acting benzodiazepines are usually used as =

A

ANXIOLYTICS

19
Q

Short acting benzodiazepines are suavely used as =

A

SEDATIVE / HYPNOTICS

20
Q

What are advantages of Bezodiazepines?

A
  • WIDE MARGIN OF SAFETY
    OVERDOSE –> PROLONGED SLEEP (but ROUSABLE)
    -IV FLUMAZENIL –> treats BZ overdose
  • MILD EFFECT ON REM SLEEP
  • DO NOT INDUCE LIVER ENZYMES
21
Q

What are unwanted effects of benzodiazepines?

A

SEDATION, CONFUSION, AMNESIA,ATAXIA (IMPAIRED MANUAL SKILLS)

POTENTIATE OTHER CNS DEPRESSANTS (ALCOHOL; BARBs)

TOLERANCE (LESS THAN BARBs; ‘TISSUE’ ONLY)

DEPENDENCE:

  • WITHDRAWAL SYNDROME SIMILAR TO BARBs (LESS INTENSE)
  • -> WITHDRAW SLOWLY
  • FREE [PLASMA] increases BY e.g. ASPIRIN, HEPARIN
22
Q

what are some other drugs used as sedatives / hypnotics ?

A

ZOPICLONE

  • ->SHORT ACTING (t½ ~ 5h)
  • -> ACTS AT BZ RECEPTORS (CYCLOPYRROLONE)
  • ->SIMILAR EFFICACY TO BZs
  • -> MINIMAL HANGOVER EFFECTS BUT DEPENDENCY STILL A PROBLEM
23
Q

what are some other drugs used as anxiolytics?

A
  • some anti depressant drugs
    SSRIs (see PT 16; Dr Croucher)
    LESS SEDATION & DEPENDENCE / DELAYED
    RESPONSE / LONG-TERM TREATMENT
  • some anti epileptic drugs
    e. g valproate, tiagabine
  • some antipsychotic drugs
    e. g. OLANZAPINE, QUETIAPINE
  • Propranolol
  • -> IMPROVES PHYSICAL SYMPTOMS
  • TACHYCARDIA (b1)
  • TREMOR (b2)
  • Buspirone
  • 5HT1A AGONIST
  • FEWER SIDE-EFFECTS (< SEDATION)
  • SLOW ONSET OF ACTION (DAYS / WEEKS)
24
Q

Benzodiazepines are used to treat ‘panic attacks’ and other anxiety states. By what mechanism do they produce their anti-anxiety effects?

A: Inhibition of GABA breakdown
B: Activation of 5HT1A receptors
C: Enhancement of the action of GABA at GABA-A receptors
D: Inhibition of GABA reuptake
E: Enhancement of the action of GABA at GABA-B receptors

A

C: Enhancement of the action of GABA at GABA-A receptors

25
Q

Which of the following drugs is commonly used in the treatment of insomnia?

A: Thiopental
B: Phenytoin
C: Baclofen
D: Sodium valproate
E: Temazepam
A

E: Temazepam

eLCRS - 팜 (36 decks)

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