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SP18: Pharm MT2 > CNS Pharmacology > Flashcards

CNS Pharmacology Flashcards

1
Q

What is the difference between typical and atypical anti-psychotics?

A

Typical - strong antagonist of D2 dopamine receptor, with little activity on D4

Atypical - antagonist on D4, less so on D2

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2
Q

What is the difference between D1, D5 receptors, and D2-4 receptors?

A

D1, D5 - activate Gs -> increase in cAMP

De2-4 - activate Gi -> decrease in cAMP

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3
Q

What do GABA receptors do?

A

Activate Cl- channels that hyperpolarize the neuron

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4
Q

What is the activity of glycine receptors?

A

Like GABA, activate Cl- channels

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5
Q

What are the differences in positive and negative symptoms?

A

Positive - hallucinations, delusions, etc.; prob linked to excess dopamine

Negative - loss of affect, catatonia; linked to prefrontal pathology

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6
Q

5-HT is a receptor for which NT?

A

Serotonin

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7
Q

What is the purpose of antipsychotics that end in -azine?

A

Block D2 receptors to reduce dopamine activity thus reducing positive schizophrenia symptoms

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8
Q

What is the glutamate hypothesis for schizophrenia?

A

Hypofunction of NMDA receptors could lead to negative symptoms

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9
Q

What is the current thoughts process in treating schizophrenia?

A

Combined 5-HT2/D2 antagonists

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10
Q

Which anti-psychotics cause the most extrapyramidal effects?

A

Typical anti-psychotics

This is why anti-typical are more popular today

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11
Q

What is the difference between sadness and depression?

A

Sadness is not chronic

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12
Q

What are the three ways that anti-depressants act?

A
  1. Block transmitter uptake
  2. Inhibit MAO
  3. Inhibit presynaptic auto-receptors
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13
Q

What are the common effects of all anti-depressants?

A

Enhance activities of dopamine, 5-HT (serotonin), and/or norepinephrine

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14
Q

What makes SSRIs better anti-depressants than TCAs?

A

SSRIs specifically block the re-uptake of serotonin

TCAs are non specific re-uptake blockers and have many more side effects

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15
Q

What are some of the significant side effects with TCAs?

A

Initial drowsiness, anxiety, confusion (goes away after several weeks)

Dry mouth, constipation, sexual dysfunction

Hypotension, arrhythmia

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16
Q

What is an SNRI?

A

Inhibits reuptake of serotonin and norepinephrine

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17
Q

How do MOAIs work?

A

Inhibit the enzyme that breaks down dopamine, 5-HT, and norepinephrine

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18
Q

T/F: MOAIs are commonly used to treat Parkinson’s.

A

True

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19
Q

__________ is an anti-depressant that blocks presynaptic autoreceptors.

A

Mirtazapine

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20
Q

What makes nefazodone, trazodone, and mirtazapine different from most anti-depressants?

A

They are serotonin receptor antagonists

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21
Q

Specifically, _________ neuron loss in the ____________ leads to Parkinson’s.

A

Dopaminergic; substantia nigra

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22
Q

Neuron loss will eventually reach a ____________ with age, and will then produce symptoms of disease.

A

Threshold

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23
Q

What happens in a normal person without Parkinson’s?

A

Activation of D2 receptors (Gi) in the striatum affects acetylcholine and GABA release

24
Q

What is the aim of Parkinson’s treatment?

A

Overcome loss of dopanergic input

25
Q

T/F: Dopamine can cross the blood-brain barrier.

A

False

L-DOPA is the drug used because it can cross the bbb; it is then converted to dopamine

26
Q

When are results from L-DOPA most notable?

A

In the first few years of treatment

27
Q

Why might L-DOPA treatments become less effective over time?

A

L-DOPA is putting more dopamine into the synapse

If there is more neurodegeneration than there will be fewer synapses at the striatum so more dopamine will not help if there are no synapses for it to be in

28
Q

What is the role of carbidopa in L-DOPA treatments?

A

It is a peripheral dopa decarboxylase inhibitor

Get more drug into CNS and prevents dopamine receptors in the gut from activating

Keeps L-DOPA as L-DOPA until in the CNS

29
Q

What are the advantages of using dopamine receptor agonists to treat Parkinson’s?

A
  1. Not as toxic as L-DOPA

2. Don’t require neuron from substantia nigra for delivery — work postsynaptically

30
Q

What is the idea behind MOA and COMT inhibitors?

A

Inhibit enzymes that break down dopamine in the synapse

31
Q

What are some adjunctive therapy options for Parkinson’s to treat specific symptoms?

A

Tremor — anticholinergic
Dyskinesias — amantadine
Off episodes — apomorphine

32
Q

What is the difference between idiopathic epilepsy and acquired epilepsy?

A

Idiopathic — inherited biochemical defect

Acquired — healed brain injury

33
Q

T/F: Phenytoin and other anti-seizure drugs block high frequency firing of action potentials.

A

True

Work in the CNS like local anesthetic works in the periphery

34
Q

Some anti-convulsants potentials the effects of ________ to dampen synaptic nerve impulses.

A

GABA

35
Q

How does vigabatrin potentiate GABA?

A

Irreversible inhibitor of GABA transaminase (normally metabolizes GABA)

36
Q

How does tiagabine potentiate GABA?

A

Inhibits GABA uptake

37
Q

What is the favored drug by dentists to treat emergency seizures? How do they work?

A

Benzodiazepines; facilitate opening of Cl- channels

38
Q

T/F: Barbituates work similarly to benzodiazepines.

A

True

Slightly less safe

39
Q

T/F: Some anticonvulsants block T-type calcium channels in the thalamus.

A

True

40
Q

What is important for dentists to know when it comes to epilepsy?

A
  1. Have emergency plan

2. Will often include Benzodiazepine

41
Q

Most anti-anxiety drugs are ______________ and _____________.

A

Barbiturates; benzodiazepines

42
Q

T/F: Benzodiazapines are much more toxic than barbiturates.

A

False

Barbiturates are more toxic

43
Q

What is the major mechanism that barbiturates and benzodiazapines use?

A

Increase Cl- conductance via action at GABA-A receptors

44
Q

What suffix do most barbiturates have?

A

-barbital

45
Q

What suffix do most benzodiazepines have?

A

-pam or -lam

46
Q

How does GABA B work differently than GABA A?

A

GABA B works through a GPCR

47
Q

___________ increase the duration of GABA-mediated Cl- channel opening. ___________ increase the frequency of GABA-mediated Cl- channel opening.

A

Barbiturates; benzodiazepines

48
Q

How are the side effects of Benzodiazepines different than Barbiturates?

A

Benzodiazepines have anti-anxiety effects at doses that don’t knock you out. Barbiturates tend to knock out everything

49
Q

When is there a risk for respiratory depression with benzodiazepines?

A

Someone is on opioids

Other than that it is very safe!

50
Q

What is the purpose of flumazenil?

A

Antagonist for benzodiazepine

Will recover from benzodiazepine overdose and recover from sedation

51
Q

What makes benzodiazepines better than tranquilizers?

A

Less potential for abuse and better therapeutic index

52
Q

___________ does not share a similar structure with benzodiazepines, but it binds to the same site and works similarly.

A

Zolpidem (ambien)

Much better for sedation

53
Q

It is thought that barbiturates specifically target which part of the brain?

A

Reticular formation

54
Q

What are the various durations for barbiturates?

A

Ultrashort: 20 mins (IV anesthesia)
Short: 3-8 hours (sedative/hypnotic)
Long: 1-2 days (anticonvulsant)

55
Q

____________ are the first line of treatment for bipolar disorder.

A

Lithium salts

56
Q

T/F: Lithium salts are best at treating the depression symptom of bipolar disorder.

A

FALSE

Treat the manic symptom

SP18: Pharm MT2 (7 decks)

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