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CNS: MDD > Sharpe's > Flashcards

Sharpe's Flashcards

1
Q

How does neurotransmission occur?

A

Neurons in the brain communicate with electrical signals with each other

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2
Q

What is the synapse?

A

The space between two neurons where neurotransmission occurs

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3
Q

What type of signal occurs between neurons?

A

Usually chemical

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4
Q

How are neurotransmitters packaged?

A
  1. vesicles
  2. active transport is needed to concentrate neurotransmitter into vesicles (antiport)
  3. Vesicular monoamine transporter (VMAT) of 5-HT, NE, & DA
  4. therapeutics can block packaging of neurotransmitter, causing their concentration in the axon terminal space to rise
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5
Q

How are neurotransmitters released?

A
  1. receives an action potential turning the electrical signal within the neuron into a chemical signal between neurons
  2. action potential induced depolarization of the membrane at the axon terminal causes the opening of calcium channels which are essential for vesicular release
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6
Q

What types of neurotransmission are there?

A

classic: neurotransmitter released from axon terminal (presynaptic) acts on either pre- or post-synaptic receptors
retrograde: neurotransmitter is released from post-synaptic neuron and acts on pre-synaptic neuron (endocavanoids not covered)

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7
Q

What types of receptors are there?

A

inotropic (ligand-gated ion channels): fast, usually POST-synaptic (ex. nicotinic ACh, GABA A receptors, glutamate receptors, glycine receptors, 5-HT3 receptors)
metabotropic (G-protein coupled receptors): slower than inotropic receptos because they work by activation of ion channels or signal cascades/2nd messenger systems, can be pre- & post-synaptic, subtype of G protein will determine excitatory (Gs) or inhibitory (Gi)

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8
Q

How does the Gs receptor activate?

A
  1. increases adenylyl cyclase activity
  2. opens Ca2+ channels
  3. inhibits Na+ channels
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9
Q

How does the Gi receptor activate?

A
  1. inhibits adenylyl cyclase activity
  2. closes Ca2+ channels
  3. opens K+ channels
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10
Q

What is the reuptake of neurotransmitters from the synapse?

A

“recycling” the neurotransmitter back into the pre-synaptic neuron (not with active transport) more with concentration gradient
ex. SERT, NET, DAT and more

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11
Q

How are neurotransmitters degraded?

A

enzymatically degradation of neurotransmitter can occur in the synapse or in the pre-synaptic terminal
degradation is one way of terminating the neurotransmitter’s action
in the pre-synaptic terminal, the degradation can decrease the amount of neurotransmitter available for packaging into vesicles

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12
Q

What is in the cerebral cortex

A

a. frontal lobe–> planning
b. motor lobe
c. speech
d. somato-sensory
e. vision, smelling, hearing

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13
Q

What is in the limbic areas?

A

a. regions: hippocampus (memory), amygdala (fear/anxiety), limbic cortex
b. functions: memory, mood, biological needs

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14
Q

What is in the midbrain?

A

a. regions: substantia nigra, basal ganglia

b. functions: movement, motivation, visual/hearing relay

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15
Q

What is in the brainstem?

A

a. regions: reticular formation, medulla, pons

b. functions: sleep/wake, attention (mainly by reticular formation), breathing, blood pressure maintenance

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16
Q

What is in the spinal cord?

A

a. connects the body to brain
b. input of peripheral information (pain & position)
c. output of central message (movement, blood pressure maintenance, body temperature maintenance, and respiration)

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17
Q

What is Glutamate?

A

glutamate= excitatory

  • uptake by astrocytes with reuptake transporters specific to glutamate (back to glutamine)
  • ionotropic receptors (FAST!) AMPA, NMDA, Kainate
  • metabotropic receptors (mGluR, SLOWER) inhibitory, so coupled to Gi
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18
Q

What is GABA?

A

GABA= inhibitory

  1. GABAa- ionotropic (binding to these receptors causes Cl- to enter cells = hyperpolarization, receptors where alcohol, barbiturates, benzodiazepines and inhalants all work)
  2. GABAb- metabotropic/G-protein coupled (can be pre or post, receptos on neurons that release glutamate, dopamine, norepinephrine or serotonin will decrease the release of THOSE neurotransmitters)
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19
Q

What are some Monoamine neurotransmitters?

A
  1. Dopamine
  2. Norepinephrine
  3. Serotonin
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20
Q

What is Dopamine?

A

Dopamine (monoamine & catecholamine)

synthesis: tyrosine hydroxylase is the rate limiting step in production of dopamine
vesicles: VMAT in the PRE-synaptic & COMT in the synapse only!
localization: cell bodies mostly limited to- ventral tegmental are (reward, addiction), substantia nigra (movement) and projections to limbic areas (emotion, memory), stratum and cortex

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21
Q

What is Dopamine reuptake?

A

Dopamine reuptake transporter (DAT)

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22
Q

What are Dopamine receptors?

A

Metabotropic
D1: coupled to Gs
D2: coupled to Gi, may be presynaptic (autoreceptors) or postsynaptic

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23
Q

What are some diseases related to Dopamine?

A

Parkinson’s disease
substance abuse
Schizophrenia
ADHD

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24
Q

What is Norepinephrine?

A

synthesis: synthesized from dopamine (dopamine betahydroxylase converts dopamine to norepinephrine)
vesicles: VMAT
degradation: MAO from presynaptic terminal & synapse & COMT in synapse only
localization: cell bodies mostly limited to (locus ceruleus & brainstem) and projections to amygdala, thalamus and cortex

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25
Q

What is Norepinephrine reuptake?

A

Norepinephrine reuptake transporter (NET)

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26
Q

What diseases are associated with Norepinephrine?

A

cognition
depression
PTSD
ADHD

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27
Q

What is Serotonin?

A

synthesis: from tryptophan
vesicles: VMAT
degradation: MAO in presynaptic terminal and synapse
localization: cell bodies limited to (raphe nucleus) and projections to limbic, midbrain and cortex

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28
Q

What is Serotonin reuptake?

A

Serotonin reuptake transporter (SERT)

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29
Q

What Norepinephrine receptors are there?

A

Metabotropic
alpha 1: coupled to Gq
alpha 2: coupled to Gi, may be presynaptic or post
beta: coupled to Gs

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30
Q

What are the types of Serotonin receptors?

A

13 different types of receptors 12 metabotropic and 1 ionotropic
5-HT3- ionotropic; antagonists at this receptor are used as anti-nausea
5-HT 1D & 1A- inhibitory, autoreceptors; agonists are used for migraine treatment
5-HT 2A- antagonists to this receptors are antipsychotic

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31
Q

What are the diseases associated with Serotonin?

A

depression
antipsychotics
migraine
obesity/weight loss

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32
Q

What is Acetylcholine?

A

synthesis: choline + acetylCoA
vesicles: vesicular acetylcholine transporter packages Ach into vesicles in axon terminal
degradation: acetylcholinesterase
localization: cell bodies in forebrain and brainstem; intrerneurons in straitum & projections to limbic areas, cortex and striatum

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33
Q

What is Acetylcholine reuptake?

A

choline transporter (only transports choline)

34
Q

What are the types of Acetylcholine receptors?

A

muscarinic: G-protein coupled receptors found in pre- & post-synapse
nicotinic: ionotropic receptors

35
Q

What are the diseases associated with Acetylcholine?

A

Alzheimer’s disease
Parkinson’s
depression

36
Q

Depression

A

persistent low mood with loss of enjoyment and pleasure

37
Q

Types of depression

A

Major depressive disorder
Dysthymia (persistent depressive disorder)
Post-partum depression
Seasonal affective disorder

38
Q

Symptoms of depression

A
  • persistent sad, anxious or “empty” feelings
  • feelings of hopelessness and/or pessimism
  • feelings of guilt, worthlessness and/or helplessness
  • irritability, restlessness
  • loss of interest in activities or hobbies once pleasurable, including sex
  • fatigue and decreased energy
  • difficulty concentrating, remembering details and making decisions
  • insomnia, early-morning wakefulness, or excessive sleeping
  • overeating or appetite loss
  • thoughts of suicide/suicide attempts
  • persistent aches or pains, headaches, cramps or digestive problems that do not ease even with treatment
39
Q

Causes of depression

A

genetics
environment (stress)
biochemical
psychological

40
Q

Monoamine Hypothesis

A

it is thought that a decrease in monoamines (5-HT & NE )is what causes depressive symptoms. if we increase monoamines, then we will be able to relieve depressive symptoms

41
Q

Neurotrophic Hypothesis

A

brain-derived neurotrophic factor (BDNF) plays a critical role in the regulation of neural plasticity, resilience and nuerogenesis of depression. less BDNF= more depressed

42
Q

What increases BDNF?

A

exercise
smiling/laughing
antidepressants
electroconvulsive therapy

43
Q

What decreases BDNF?

A

stress

pain

44
Q

Which of the following neurotransmitters are most closely associated with depression?

a. ACh
b. DA
c. GABA
d. glutamate
e. NE
f. 5-HT

A

DA, NE & 5-HT

45
Q

Selective Serotonin Reuptake Inhibitors (SSRI’s)

A 
Fluoxetine (Prozac)
Citalopram (Celexa)
Escitalopram (Lexapro)
Sertraline (Zoloft)
Paroxetine (Paxil) 
Fluvoxamine (Luvox) **treats OCD
46
Q

General side effects of SSRI’s

A
  • *all side effects are dose dependent and want to keep patient on the lowest dose possible
  • GI effects: 5-HT3 mediated, nausea
  • Stimulation and anxiety: (except paroxetine), insomnia & agitation
  • Sexual dysfunction: 5-HT2 activity, both in men and women
  • headaches: levels fluctuate causing headaches
47
Q

Alcohol and SSRI’s

A

alcohol may worsen depressive symptoms and cause increased sedation

48
Q

Discontinuation Syndrome

A 
dizziness
nausea
anxiety
agitation
lethargy
**short t 1/2 = more problems (paroxetine)
49
Q

Suicide risk

A

patients under 25 yo at greatest risk

rare over 65 yo

50
Q

SSRI selectivity of action

A

***all block SERT
Fluoxetine (Prozac): has + 5-HT2 (sexual)
Paroxetine (Paxil): has + NET & + ACh M

51
Q

Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRI’s)

A 
Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)
Duloxetine (Cymbalta)
Milnacipran (Savella)
Levomilnacipran (Fetzima)
52
Q

General side effects of SNRI’s

A 
sexual dysfunction
nausea
insomnia (CNS stimulation)
increase blood pressure possible
discontinuation syndrome (dose dependent)
53
Q

SNRI selectivity of action

A

***all block SERT & NET
Venlafaxine (Effexor): less NET
Duloxetine (Cymbalta): less SERT

54
Q

Norepinephrine and Dopamine Reuptake inhibitors (NDRI’s)

A

Bupropion (Wellbutrin, Zyban, Wellbutrin XL, Wellbutrin SR)

55
Q

What does Bupropion do?

A
  • it resembles amphetamine, blocks NET & DAT= increase in concentration of NE & DA
  • *no 5-HT activity!
  • do not use for epileptics (lowers seizure threshold)
  • do not use if patient is on an MAO inhibitor = increase NTs and no way of getting rid of them
56
Q

Bupropion side effects

A 
anxiety
insomnia (CNS stimulation)
seizures
hypertension
hallucinations/psychosis (with increase DA)
57
Q

Does Bupropion cause sexual dysfunction or weight gain?

A

No it will not because those symptoms are more pronounced when dealing with Serotonin (5-HT)

58
Q

Tricyclic Antidepressants (TCA’s)

A 
Amitriptyline (Elavil)
Nortriptyline (Pamelor)
Doxepine (Sinequan)
Imipramine (Tofranil)
Clomipramine (Anafranil)
Desipramine (Norpramin)
59
Q

Major concerns of TCA’s

A

cardiac toxicity (especially in kids): due to sodium channel blockade
seizures
discontinuation syndrome
side effects differ by drug

60
Q

General side effects of TCA’s

A

anti-histaminergic: sedation, confusion, increased appetite
anti-muscarinic: anti-SLUD effects (can’t pee, dry mouth)
adrenergic alpha1 antagonism: orthostatic hypotension

61
Q

TCA’s selectivity of action

A

Doxepine (Seniquan): (+) SERT, NET, 5-HT2 (++) ACh M, (+++) H1 & alpha1
Imipramine (Tofranil) : (+) NET, 5-HT2, H1, alpha1 (++) SERT & AChM
Desipramine (Norpramin): (+) 5-HT2, H1, ACh M, alpha1, & SERT (+++) NET
Clomipramine (Anafranil): (+) 5-HT2, H1, ACh m (++) NET & alpha1 (+++) SERT
Amitriptyline (Elavil): (+) NET & 5-HT2(++) SERT & H1 (+++) ACh M & alpha1
Nortriptyline (Pamelor): (+) SERT, 5-HT2, H1, ACh M, & alpha1 (++) NET

62
Q

Monoamine Oxidase Inhibitors

A

Isocarboxazid (Marplan)
Phenelzine (Nardil)
Selegiline (Eldepryl) **patch
Tranycypromine (Parnate)

63
Q

MAO A

A

high affinity for NE and 5-HT; found in the brain, gut and liver

64
Q

MAO B

A

more centrally located, metabolizes DA and other monoamines

65
Q

General information about MAO

A
  • the lifespan of an MAO is about 2-3 weeks

- inhibitors available are IRREVERSIBLE and largely non-specific

66
Q

MAO inhibitor issues of concern

A

Serotonin syndrome: caused by high levels of serotonin

  • twitching muscles
  • irregular or high heart rate
  • high fever
  • agitation, headache
  • diarrhea
  • seizures
67
Q

When does Serotonin Syndrome happen?

A

when we use an MAOI with anything that will increase serotonin levels, for example SSRI’s, SNRI’s, TCA’s. You wouldn’t see it with bupropion because it does not have anything to do with serotonin

68
Q

Hypertensive Crisis

A

acute onset of severe throbbing headache, possibly accompanied by blurred vision, palpitations, chest pain and shortness of breath

69
Q

How does hypertensive crisis happen?

A
  • time from ingestion of tyramine containing food to symptoms = minutes
  • tyramine containing foods aren’t metabolized by MAI and since MAOI’s are being used absorbed tyramine from the gut displace NE in vesicles causing increased levels
70
Q

What are tyramine containing foods?

A

beer (alcoholic and non-alcoholic), red wine, aged cheese, pickled/fermented foods, overripe fruit (raisins, bananas), aged meats (salami, pepperoni, etc)

71
Q

Can you take Pseudoephedrine while on an MAOI?

A

No any sypathomimetics (cocaine, amphetamine, etc) can add to the hypertensive crisis

72
Q

Other side effects of MAOI’s

A 
orthostatic hypertension (takes 3-4 weeks to see due to remodeling)
weight gain
sexual dysfunction
73
Q

Discontinuation or Switching of MAOI’s

A

washout required for MAOI’s!
switching away from MAOI = 2 weeks
moving to an MAOI depends on t 1/2 life of other drug that increases 5-HT levels

74
Q

MAOI selectivity of action

A

***all block MAO A & B

75
Q

Atypical Antidepressants

A 
Mirtazapine (Remeron)
Trazodone (Desyrel)
Nefazodone (Serzone)
Vilazodone (Viibryd)
Vortioxetine (Trintellix/Brintellix)
76
Q

Mirtazapine (Remeron)

A
  • alpha2 antagonist (increases release of NE and 5-HT
  • antagonist 5-HT2 & 5-HT3 (direct) and AGONIST at 5-HT1A receptor (indirect)
    ADR: weight gain, dry mouth, sedation
    less sexual dysfunction and nausea than others
77
Q

Trazodone (Desyrel) & Nefazodone (Serzone)

A
  • antagonists at 5-HT2R, inhibition of SERT at higher doses
    Nefazodone- BBW liver toxicity
    ADR: sedation (anti-histaminic activity), orthostatic hypotension (antagonist @ alpha1 receptor), priapism (trazodone especially)
    **low risk of sexual dysfunction due to 5-HT2 antagonism
78
Q

Vilazodone (Viibryd)

A
  • selective SERT inhibitor
  • 5-HT 1A partial agonist
    ADR: nausea and diarrhea
79
Q

Vortioxetine (Trintellix/Brintellix)

A
  • selective SERT inhibitor
  • 5-HT 1A receptor agonist, 5-HT3 receptor antagonist
    ADR: sexual dysfunction
80
Q

Atypical antidepressant selectivity action

A

Mirtazapine (Remeron): (+) 5-HT2, (+++) H1, other alpha2 antagonist, 5-HT1 indirect agonist, 5-HT3 antagonist
Trazodone (Desyrl): (+) SERT & H1 (++) 5-HT2 & alpha1
Nefazodone (Serzone): (+) SERT, NET, alpha1 (++) 5-HT2
Vilazodone (Viibryd): (++) SERT, other 5-HT1A partial agonist
Vortioxetine (Trintellix/Brintellix): (++) SERT, other 5-HT1A agonist, 5-HT# antagonist

81
Q

Delayed Therapeutic Effect

A

therapeutic effect lags behind about 2-8 weeks.
Possible causes:
- receptor down regulation
- uptake of 5-HT by other transporters
- downstream effects (gene transcription or neurogenesis)

CNS: MDD (2 decks)

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