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CNS: MDD > Sharpe's > Flashcards

Sharpe's Flashcards

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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
What is Norepinephrine reuptake?
Norepinephrine reuptake transporter (NET)
26
What diseases are associated with Norepinephrine?
cognition depression PTSD ADHD
27
What is Serotonin?
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
28
What is Serotonin reuptake?
Serotonin reuptake transporter (SERT)
29
What Norepinephrine receptors are there?
Metabotropic alpha 1: coupled to Gq alpha 2: coupled to Gi, may be presynaptic or post beta: coupled to Gs
30
What are the types of Serotonin receptors?
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
31
What are the diseases associated with Serotonin?
depression antipsychotics migraine obesity/weight loss
32
What is Acetylcholine?
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
33
What is Acetylcholine reuptake?
choline transporter (only transports choline)
34
What are the types of Acetylcholine receptors?
muscarinic: G-protein coupled receptors found in pre- & post-synapse nicotinic: ionotropic receptors
35
What are the diseases associated with Acetylcholine?
Alzheimer's disease Parkinson's depression
36
Depression
persistent low mood with loss of enjoyment and pleasure
37
Types of depression
Major depressive disorder Dysthymia (persistent depressive disorder) Post-partum depression Seasonal affective disorder
38
Symptoms of depression
- 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
Causes of depression
genetics environment (stress) biochemical psychological
40
Monoamine Hypothesis
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
Neurotrophic Hypothesis
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
What increases BDNF?
exercise smiling/laughing antidepressants electroconvulsive therapy
43
What decreases BDNF?
stress | pain
44
Which of the following neurotransmitters are most closely associated with depression? a. ACh b. DA c. GABA d. glutamate e. NE f. 5-HT
DA, NE & 5-HT
45
Selective Serotonin Reuptake Inhibitors (SSRI's)
``` Fluoxetine (Prozac) Citalopram (Celexa) Escitalopram (Lexapro) Sertraline (Zoloft) Paroxetine (Paxil) Fluvoxamine (Luvox) **treats OCD ```
46
General side effects of SSRI's
* *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
Alcohol and SSRI's
alcohol may worsen depressive symptoms and cause increased sedation
48
Discontinuation Syndrome
``` dizziness nausea anxiety agitation lethargy **short t 1/2 = more problems (paroxetine) ```
49
Suicide risk
patients under 25 yo at greatest risk | rare over 65 yo
50
SSRI selectivity of action
***all block SERT Fluoxetine (Prozac): has + 5-HT2 (sexual) Paroxetine (Paxil): has + NET & + ACh M
51
Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRI's)
``` Venlafaxine (Effexor) Desvenlafaxine (Pristiq) Duloxetine (Cymbalta) Milnacipran (Savella) Levomilnacipran (Fetzima) ```
52
General side effects of SNRI's
``` sexual dysfunction nausea insomnia (CNS stimulation) increase blood pressure possible discontinuation syndrome (dose dependent) ```
53
SNRI selectivity of action
***all block SERT & NET Venlafaxine (Effexor): less NET Duloxetine (Cymbalta): less SERT
54
Norepinephrine and Dopamine Reuptake inhibitors (NDRI's)
Bupropion (Wellbutrin, Zyban, Wellbutrin XL, Wellbutrin SR)
55
What does Bupropion do?
- 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
Bupropion side effects
``` anxiety insomnia (CNS stimulation) seizures hypertension hallucinations/psychosis (with increase DA) ```
57
Does Bupropion cause sexual dysfunction or weight gain?
No it will not because those symptoms are more pronounced when dealing with Serotonin (5-HT)
58
Tricyclic Antidepressants (TCA's)
``` Amitriptyline (Elavil) Nortriptyline (Pamelor) Doxepine (Sinequan) Imipramine (Tofranil) Clomipramine (Anafranil) Desipramine (Norpramin) ```
59
Major concerns of TCA's
cardiac toxicity (especially in kids): due to sodium channel blockade seizures discontinuation syndrome side effects differ by drug
60
General side effects of TCA's
anti-histaminergic: sedation, confusion, increased appetite anti-muscarinic: anti-SLUD effects (can't pee, dry mouth) adrenergic alpha1 antagonism: orthostatic hypotension
61
TCA's selectivity of action
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
Monoamine Oxidase Inhibitors
Isocarboxazid (Marplan) Phenelzine (Nardil) Selegiline (Eldepryl) **patch Tranycypromine (Parnate)
63
MAO A
high affinity for NE and 5-HT; found in the brain, gut and liver
64
MAO B
more centrally located, metabolizes DA and other monoamines
65
General information about MAO
- the lifespan of an MAO is about 2-3 weeks | - inhibitors available are IRREVERSIBLE and largely non-specific
66
MAO inhibitor issues of concern
Serotonin syndrome: caused by high levels of serotonin - twitching muscles - irregular or high heart rate - high fever - agitation, headache - diarrhea - seizures
67
When does Serotonin Syndrome happen?
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
Hypertensive Crisis
acute onset of severe throbbing headache, possibly accompanied by blurred vision, palpitations, chest pain and shortness of breath
69
How does hypertensive crisis happen?
- 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
What are tyramine containing foods?
beer (alcoholic and non-alcoholic), red wine, aged cheese, pickled/fermented foods, overripe fruit (raisins, bananas), aged meats (salami, pepperoni, etc)
71
Can you take Pseudoephedrine while on an MAOI?
No any sypathomimetics (cocaine, amphetamine, etc) can add to the hypertensive crisis
72
Other side effects of MAOI's
``` orthostatic hypertension (takes 3-4 weeks to see due to remodeling) weight gain sexual dysfunction ```
73
Discontinuation or Switching of MAOI's
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
MAOI selectivity of action
***all block MAO A & B
75
Atypical Antidepressants
``` Mirtazapine (Remeron) Trazodone (Desyrel) Nefazodone (Serzone) Vilazodone (Viibryd) Vortioxetine (Trintellix/Brintellix) ```
76
Mirtazapine (Remeron)
- 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
Trazodone (Desyrel) & Nefazodone (Serzone)
- 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
Vilazodone (Viibryd)
- selective SERT inhibitor - 5-HT 1A partial agonist ADR: nausea and diarrhea
79
Vortioxetine (Trintellix/Brintellix)
- selective SERT inhibitor - 5-HT 1A receptor agonist, 5-HT3 receptor antagonist ADR: sexual dysfunction
80
Atypical antidepressant selectivity action
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
Delayed Therapeutic Effect
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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