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Module 4: Neuro > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the different groups of antidepressants?

A
  1. Tricyclic antidepressants (TCAs)
  2. Seratonin Specific Reuptake Inhibitors (SSRIs)
  3. Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs)
  4. Monoamine oxidase inhibitors (MAOIs)
  5. . Atypical (heterocyclic second and third gen) antidepressants
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2
Q

What is the mechanism of action for Tricyclic antidepressants (TCAs)?

A
  • Inhibit transporters of NE and 5HT
  • Inhibit reuptake of NE and 5HT
  • Results in potentiation of NT action (adrenergic and serotonergic) and enhancement of post synaptic response
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3
Q

What is the mechanism of action for SSRI’s?

A
  • Inhibit serotonin transporter
  • Lead to increased serotonin neurotransmission
  • highly selective, reduced side effect profile
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4
Q

What are side effects of SSRI’s?

A
  • Gastrointestinal (nausea and vomiting)
  • Sexual dysfunction (decreased libido and ED)
  • Headache
  • Agitation
  • Together with TCAs or MAOIs can get serotonin syndrome
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5
Q

What can cause seratonin syndrome?

A

Caused by overactivation of sertinergic neurotransmission through interaction of two classes of drugs that can influence seratonin levels:

SSRI
TCA
MAOI

–> should not be prescribed together, wait 2-3 weeks after stopping MAOI to switch to TCA or SSRI

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6
Q

What are symptoms of seratonin syndrome?

A

Cognitive, autonomic and somatic effects:

Muscle rigidity
myoclonus
hyperthermia
cardiovascular instability
CNS stimulatory effects including confusion, hypomania, hallucinatiosn, seizures

Can be life threatening

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7
Q

What drugs are Tricyclic antidepressants?

A

Tertiary amines (SERT > NET)
Amitriptyline
Imipramine

Secondary amines (NET > SERT)
Nortryptyline
Desipramine

Others
Clomipramine
Doxepin
Amoxapine

End in -iptyline or -ipramine except doxepin and amoxapine

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8
Q

What drugs are SSRIs?

A

Fluoxetine

Paroxetine

Sertraline

Fluvoxamine

Citalopram

Excitalopram

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9
Q

What is the mechanism of SNRIs?

A

Inhibition of serotonin and NE reuptake
(Inhibit SERT and NET)

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10
Q

What drugs are SNRIs?

A

Venlafaxine

Duloxetine

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11
Q

What is the clinical use of SNRIs?

A

Depression

generalized anxiety disorder (Venlafaxine)

diabetic peripheral neuropathy (duloxetine)

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12
Q

What are clinical uses of SSRIs?

A

Major Depression

Bedwetting (imipramine)

OCD (clomipramine)

fibromyalgia

Bulimia

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13
Q

What is Bupropion?

A

Atypical antidepressant

Acts as a dopamine and NE reuptake inhibitor

Also used to treat:
Nicotine withdrawal
ADHD
Bipolar depression

Side effects:
Dry mouth
nausea
Insomnia
No sexual side effects

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14
Q

What is Trazodone?

A

Atypical antidepressant

- Primarily inhibits seratonin reuptake

Used to treat:
Depression (high dose)
Insomnia

Side effects:
Orthostatic hypotension
Nausea
Dizziness
Sedation
Priapism (Trazobone)

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15
Q

What is Mirtazapine?

A

Atypical Antidepressant

- alpha2 antagonist (on presynaptic cells) results in increased release of NE and serotonin
Potent 5HT2 and 5HT3 receptor antagonist (seratonin reuptake inhibitor)

Side effects:
Sedation
Increased appetite
Weight gain
Dry mouth

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16
Q

What is Vilazodone?

A

Atypical antidepressant

FDA approved in 2011

Mechanism of Action: Combined SSRI and 5HT1A partial agonist

Side effects:
Little sexual dysfunction
Mainly GI related: Nausea, diarrhea

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17
Q

What do TCAs inhibit that SSRIs do not inhibit?

A

Norepinephrien Reuptake transporter (NET)

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18
Q

What is the mechanism of action for MAOIs?

A
  • Irreversible inhibitors of MAO-A and MAO-B
  • MAOs degrade monoamine and catecholamine NTs in brain
  • Inhibiting degradation of NTs leads to build up in cytoplasm, and uptake into storage vesicles
  • Also results in leakage of NE and 5HT into synaptic cleft

–> Increased monoamine neurotransmission

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19
Q

What are side effects of MAOIs?

A

Hypertensive crisis with tyramine ingestion (in wine and cheese) and ß-agonists

Sedation or excitation

postural hypotension

Can induce mania in some bipolar patients

Contraindicated with SSRIs or meperidine (to prevent seratonin syndrome)

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20
Q

What are the clinical uses of MAOIs?

A

atypical depression
(Antidepression of choice for this)

Anxiety

Hypochondriasis

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21
Q

What are the risks of taking antidepressants during pregnancy for SSRIs

A
  • *SSRI:**
  • Appear to be “relatively” safe - though always some risk
  • Use in 3rd trimester may cause withdrawal symptoms and increased risk of persistent pulmonary hypertension in newborn
  • *Paroxetine:**
  • the exception: slight increased risk of heart defects in fetus
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22
Q

What are the risks of not taking antidepressants during pregnancy?

A

Pre-term labor

low birth weight infants

problems with bonding

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23
Q

What can be used to augment antidepressant efficacy?

A
  • Lithium
  • Thyroid hormones
  • *Antipshycotics:**
  • Aripiprazole
  • Olanzapine
  • Quetiapine
  • *Anti-anxiety:**
  • Buspirone
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24
Q

What classes of drugs are used to treat bipolar disorders?

A

Mood stabilizers
Lithium
Carbamazapine
Valproate
Lamotrigine

Anti-psychotics
Chlorprmazine
Haloperidole
Olanzapien
Risperidone

Antidepressants
SSRI
Buproprion

25
What is the mechanism of action of lithium?
Precise mechanism as a mood stabilizing agent unknown Possibly related to inhibition of phophoinositol cascade (which inhibits glycogen synthase kinase)
26
What are clinical uses of lithium?
Mood stabilizer for bipolar disorder Blocks relapse of acute manic events Also, SIADH
27
What are side effects of lithium?
* *LMNOP:** * *L**ithium side effects: **M**ovement (tremor) **N**ephrogenic diabetes insipidus Hyp**O**thyroidism **P**regnancy problems Also: Excessive thirst Urinary frequency and increased volume Memory problems Weight gain Drowsiness Diarrhea
28
What is used to treat acute mania?
Antipsychotics (mood stabilizers don't act fast enough to be monotherapy for severe mania) Neuroleptic: **haloperidol** Atypical antipsychotic: **olanzapine, risperidone**
29
What are the different ester local anesthetics?
Cocaine Procaine Tetracaine Benzocaine
30
What are the different amide local anesthetics?
Lidocaine Bupivacaine
31
What is the general structure of local anesthetics?
**Lipophilic group** (usually aromatic ring) attached to **Intermediate chain ** (ester or amide) attached to **Hydrophilic group** (usually 2° or 3° amine) Exception: Benzocaine doesn't have a hydrophilic group
32
How do effects of esters differ from amides?
In general: Increased hydrophobicity Increased anesthetic potency Increased duration of action Increased toxic side effects
33
Where is the binding site for local anesthetics?
Intracellular region of the Na+ channel pore during the Intermediate closed conformation, open conformation, or inactivated conformation - Na+ channel has low affinity for LA during resting conformation
34
How does the local anesthetic enter the cell?
- Unprotonated, uncharged form of LA will access the LA binding site (on intracellular region of Na+ channel) by diffusing through cell membrane --\> Once inside the cell, the ionized form does not easily pass through the cell membrane - Infected tissue is generally more acidic, and AL are less able to cross membranes (they become protonated)
35
What is the mechanism of action by local anesthetics?
Block increases in Na+ permeability responsible for conduction in excitable membranes Results in: Increased AP threshold Decreased AP rate of rise and amplitude
36
What allows for persistence of function and some pressure sensitivities when under local anesthetics (i.e. moving jaw and feeling dentist pushing against your jaw after a nerve block)?
**Differential nerve block:**
37
What is the level of nerve susceptibility and the order of sensations lost under a differential nerve block by local anesthetic?
Susceptibility to block: **C \> A(delta) \> A(gamma) \> Aß \> A(alpha)** Sensations lost in order: **Pain --\> Temperature --\> Touch --\> Deep pressure --\> motor** Sensations regained in reverse order
38
What affects a nerve's susceptibility to a differential nerve block by local anesthetics?
**1. Myelination:** Nerves with shorter critical lengths (i.e. C fibers) are blocked before those with longer critical lengths (i.e. A fibers) Increased myelination leads to less Na+ channels being affected by the LA **2. Firing Frequency:** Nerves with faster firing frequency are block before those with slower firing frequency Sensory nerves fire faster than motor nerves **3. Fiber Position:** Outer nerves are infiltrated before inner nerves
39
What influences absorption of local anesthetics?
Dose Vascularity of injection site Inclusion of vasoconstrictor Chemical properties of LA
40
What is the first step to clearing local anesthetics from the body?
They are cleared from the body following systemic absorption
41
How do vasoconstrictors affect local anesthetic absorption?
They prevent blood flow to the injection site, thus slowing absorption and prolonging duration of action and decreasing systemic distribution/toxicity
42
How do the chemical properties of bupivacaine affect it's systemic absorption?
Bupivacaine is more lipid soluble than other local anesthetics (i.e. lidocaine) - It's a more potent agent with less systemic absorption over time - It takes longer to be cleared form the body
43
How are ester-type local anesthetics metabolized?
Hydrolyzed **very rapidly** by plasma cholinesterase - many metabolized to p-aminobenzoic acid (PABA) \*Exception: cocaine is metabolized in liver and plasma and parially excreted, unchanged, in urine
44
How are amide-type local anesthetics metabolized?
Metabolized **slowly** by liver microsomal CYP450 (no PABA metabolites) slower metabolism = greater chance of toxicity
45
What are CNS side effects of local anesthetics?
**Stimulation --\> Seizures --\> Depression --\> Death** Even though they are anesthetics, stimulation is a side effect b/c they will inhibit the inhibitory circuits 1st --\> leading to increased excitation **pre-treat with benzodiazepine if using high doses of LA** \*Cocaine also produces mood and behavioral changes
46
What are cardiovascular side effects of local anesthetics?
LA block all excitable tissues, including cardiac and smooth muscle: **- Decreased myocardial electrical excitability and conduction rate** **- Decreased blood pressure via reduced myocardial contraction strength and arteriolar dilation** * *- Low doses: antiarrhythmic - High doses: causes arrhythmia** \*Cocaine increases HR and BP due to intrinsic sypathomimetic and vasoconstrictive properties
47
What are neurological effects of local anesthetics?
**Direct neurotoxicity** Dependent on LA dose and length of exposure --\> can directly injure the neuron vasoconstrictors can potentiate neurotoxicity **Can do the same for muscles: direct myotoxicity**
48
How can local anesthetics affect the body's blood supply and subsequent oxygen supply?
**Methemoglobinemia** (rare-topical benzocaine) Metabolized to oxidizing agent o-toluidine, which can convert hemoglobin to methemoglobin - Abnormal levels of oxidized hemoglobin cannot bind and transport oxygen **Symptoms:** Chocolate cyanosis anxiety, fatigue, tachycardia coma and death **Treatment:** Not always necessary (spontaneous conversion may be adequate) ALWAYS remove causitive agent Reducing agents (i.e. methylene blue or ascorbic acid) may be used to treat
49
What hypersensitivity reactions can occur due to local anesthetics?
Allergic dermitis asthmatic attack anaphylactic rxn --\> risk is greater with ester- than amid-type due to formation of PABA metabolites - Cross sensitivity can occur within a class, no cross-sensitivity btwn classes
50
What are drug interactions of local anesthetics?
- PABA metabolites of many ester-type LA inhibit actions of **sulfonamide antibiotics** **- Neuromuscular blockers**
51
What are possible toxicities of cocaine?
Cell degeneration and necrosis Snorting can lead to nasal septum degeration and necrosis (due to constant vasoconstriction) Injection can lead to local necrosis near injection site (also due to vasoconstriction)
52
What are clinical uses of local anesthetics? What are possible advantages/disadvantages?
**Topical**: Surface application of LA to skin or mucous membrane -- \*anesthesia is superficial only\* due to rapid systemic absorption **Injection** **Infiltration****:** Injection of LA directly into tissue; no consideration of cutaneous nerves Advantage: **no disruption of bodily function** Disadvantage: **Need a lot of anesthetic for small area** **Field Block**: Injection of LA around border or proximal to field needing anesthesia Advantage: **no disruption of surgical field** **Nerve block:** injection of LA adjacent to nerve supplying field needing anesthesia **Epidural:** Injection of LA into epidural space, cervical, thoracic, lumbar, or sacral **Spinal** **/ Intrathecal**: Injection of LA into CSF in lumbar region Popular for surgery involving lower abdomen, extremeties, perineum Often combined with IV sedatives and amnetics
53
What are two examples of toxins that reversibly block Na+ channels?
**Tetrodotoxin**: puffer fish some poisonous newts and frogs **Saxitoxin:** dinoflagellates that cause "red tide" **\*No antidote and extremely potent - can cause fatal poisoning** **Receptor site = outer mouth of Na+ channel pore**
54
What does morphine inhibit that allows it to diminish anxiety and dread associated with pain?
**mu opoid receptors** on cell bodies and on fibers of the locus ceruleus neurons
55
What is enkephalin?
Inhibitory NT released from neurons in the periaquaductal gray matter to inhibit pain fibers that prject from PAG to the raphe nucleus enkephalin activates the mu poiod recpetors resulting in: Increase of K+ efflux Decrease in Ca2+ influx --\> Depolarization of primary pain fiber is arrested by hyperpolarization of terminal and Glu release is prevented by blockade of Ca2+ entry
56
What is seratonin?
57
What do tricyclic antidepressants end in?
- ptyline - ipramine except: doxipin and amoxapine
58
What do amide local anestetics end in?
-caine with "i" before caine (total of 2 "i"'s)

Module 4: Neuro (17 decks)

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