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Neuro / Psych SketchyPharm Flashcards

1
Q

Which benzos do not require microsomal monooxygenases to work?

A 
OTL = Outside The Liver (still technically conjugated in the liver but do not require the slow Phase I reactions)
O = oxazepam
T = temazepam 
L = lorazepam
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2
Q

Is Triazolam long or short acting?

A

Short-acting, high addictive potential like alprazolam, oxazepam, and midazolam

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3
Q

What effect do benzos have on REM sleep?

A

Like alcohol, they decrease REM sleep

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4
Q

Are the three Z’s good for sleep maintenance?

A

No - they have a rapid onset of action but also a short halflife, reducing tolerance but at the same time only making them good for inducing sleep (maybe with the exception of eszopiclone which has a slightly longer halflife)

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5
Q

What is the firstline treatment of neonatal seizures?

A

Phenobarbital

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6
Q

How is essential tremor treated?

A

Drugs: Nonselective beta blockers + primidone (think of the lady getting a perm and combed with a shaking hand)

Self-medication: Transient suppression by alcohol
(also mediates GABA, like primidone)

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7
Q

What are the mechanisms of etomidate and propofol? What are the adverse effects?

A

Both potentiate GABA-A (think of the cab in the back)

Propofol - profound respiratory depression / hypotension
-> not good for those who aren’t hemodynamically stable

Etomidate - stable in those with cardiovascular risk, but profound nausea / vomiting post-op.

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8
Q

In what “state” are patients in when they take ketamine?

A

Cataleptic state - it is a dissociative agent - causes nystagmic gaze with eyes open
-> NMDA antagonist

Hallucinogen and irrational behavior during recovery

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9
Q

What are the advantages of ketamine?

A

Good analgesia, amnesia, and hypnosis. Can be used to induce or sustain anesthesia in patients with CV problems

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10
Q

How does blood:gas partition coefficient relate to induction speed, recovery time, potency, and MAC?

A

Increased blood:gas partition coefficient = increased solubility in blood = slower rate of rise to reach mass = slower induction speed

Also, since more gas will be soluble in blood = takes longer to clear from blood = longer recovery time.

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11
Q

How does oil:gas partition coefficient relate to induction speed, recovery time, potency, and MAC?

A

Increased solubility in lipids = increased potency = lower minimum alveolar concentration required to induce (potency is inversely proportional to MAC)

Lipid solubility has no relation to induction speed / recovery time

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12
Q

What does MAC mean?

A

Minimal alveolar concentration (ED50) - the concentration of inhaled anesthetic required to prevent 50% of patients from moving in response to noxious stimuli (MACs are additive btw, so you can give two adjacents at 0.5 their MACs and produce 1.0 MACs worth of sedation).

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13
Q

What is the order of anesthetic equilibration within the tissues? How do these compartment sizes differ)

A

Highly perfused tissues equilibrate first -> brain, heart, kidney, liver (small compartment)

Medium blood flow second -> muscles (medium size)

Low blood flow last -> fat (largest size)

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14
Q

What are the organ systemic effects of inhalation anesthetics (IA) and which one is the exception? Think CV, respiratory, brain, kidney, and liver.

A

Nitrous oxide is the exception

CV - drop in blood pressure by various mechanism
Respiratory - decreased minute ventilation, hypercapnia
Brain - Increased blood flow (increases ICP)
Kidney - Decreased RBF / GFR
Liver - Decreased hepatic blood flow

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15
Q

What is the primary toxicity of concern with nitrous oxide?

A

By inactivating methionine synthase, it can halt DNA production, leading to bone marrow depression and even pernicious anemia (B12-dependent enzyme)

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16
Q

What is the unique risk incurred by usage of halothane?

A

Hepatotoxicity - “H” - it is metabolized in liver, and can lead to trifuoloracetylated proteins which are hepatotoxic and can cause hepatitis / necrosis
-> centrilobular necrosis (Zone 3)

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17
Q

Which IAs are most likely nephrotoxic and what is its mechanism?

A

Sevoflurane -> metabolism in liver leads to the formation of inorganic fluoride ions

Also NEPHrotoxic = METHoxyflurane

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18
Q

What inhaled anesthetic is most likely to cause seizures?

A

Enflurane = Epileptogenic (think of the shaking pinata)

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19
Q

What agent other than the inhaled anesthetics can cause malignant hyperthermia? What is the mechanism? Treatment?

A

Succinylcholine. Remember than N20 can’t cause this however.

Susceptible: Autosomal dominant mutation in RyR (voltage-sensitive Ca+2 channel). (think of RYAN)
-> excessive release in Ca+2 (due to mutation) results in excessive SERCA activity which generates excessive heat
Treatment: Dantrolene - RyR antagonist

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20
Q

Are local anesthetics analgesics?

A

No, they are not specific inhibitors of the pain pathway (i.e. opioid analgesics). They just nonspecifically inhibit the conduction of action potentials

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21
Q

What form of the local anesthetic (LA) is active and how does it work? That is, what is the mechanism of action?

A

Only the protonated form -> binds to the LA binding site on the OPEN sodium channel and stabilizes the inactive state of the channel

Extends refractory period by delaying return to closed / resting conformation (occurs in a progression from increased threshold to total action potential abolishment)

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22
Q

What lipid solubility profile for a LA is most clinically effective and why?

A

Moderate hydrophobicity

Too low - hydrophilic molecules cannot cross to interior of membrane

Too high - hydrophobic molecules will get stuck in the membrane and not want to enter the cellular cytoplasm

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23
Q

What does the pKa of the given local anesthetic determine? What is their relative pKa range?

A

The time of onset. All are weak bases overall -> protonated form is the charged form, with pkas between 8-9

Low pKa = LA is relatively acidic, will easier lose proton exist in deprotonated and uncharged form -> rapid crossing of membrane and rapid onset

High pKa = LA is relatively basic, will exist in protonated form which is charged -> slow crossing of membrane and slower onset

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24
Q

What are three examples of regional anesthesia procedures?

A
  1. Spinal anesthesia - injection into lumbar cistern for lower abdominal, pelvic, rectal, or orthopedic surgery
  2. Epidural anesthesia - Injection into epidural space -> for childbirth / labor
  3. Nerve block - injection around nerve truck for site distal to surgery -> i.e. brachial plexus for hand surgery
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25
Q

What are the types of A and C fibers and what information do they carry? How do they relate with respect to diameter / myelination?

A

A = heavily myelinated, in order of descending diameter
A-alpha - unconscious proprioception, motor
A-beta - DC-ML = fine touch, pressure
A-gamma - intrafusal spindle information
A-delta - ALS - acute pain, temperature

C= unmyelinated, small diameter
C - ALS - slow, aching and burning

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26
Q

For a local anesthetic, is it easier to block a myelinated or unmyelinated nerve, and a small or large nerve? Is nerve size or myelination more important?

A

Myelinated nerve -> only needs to block 3 consecutive nodes of Ranvier to block saltatory conduction

Small diameter nerve -> electrical field travels farther on sections of larger nerve, and the nodes of a large nerve will be much farther apart (need a wider area of anesthetic to cover)

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27
Q

Would a small, unmyelinated nerve or large, myelinated nerve be blocked first?

A

Size is more important, meaning a small, unmyelinated nerve will be blocked before a large, myelinated nerve.

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28
Q

What is often done to prevent toxicity of LA?

A

Reduce blood flow to the area of injection and reduction in systemic circulation by injection with epinephrine

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29
Q

How are ester LA’s metabolized? How about amides?

A

Esters - Via pseudocholinesterase enzymes in the plasma, very rapidly, with metabolites excreted in urine

Amides - Via CYP450’s in liver

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30
Q

What are the toxic effects of LA in the CNS and what is done prophylactically?

A

CNS stimulation by depressing cortical inhibition pathways

-> dizziness, tremors, metallic taste, confusion, respiratory depression

Premedicate with benzodiazepines

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31
Q

What are the cardiovascular effects of LA’s?

A

By blocking SANS conduction, they result in decreased cardiac output and arteriolar vasodilation (except cocaine) -> hypotension

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32
Q

What class of LA’s is most likely to cause an allergic reaction and why?

A

Esters -> derivatives of p-aminobenzoic acid (PABA)

If allergic to esters, give amides

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33
Q

List the clinically important amide LA’s?

A

Drugs containing ‘i’ before the caine (two I’s in the name)

  1. Lidocaine
  2. Bupivacaine
  3. Ropivacaine
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34
Q

What is the toxicity of concern with benzocaine? Is it an amide or an ester?

A

Benzocaine - ester (not two I’s)

Toxicity - Methemoglobinemia -> treat with methylene blue

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35
Q

Why would bupivacaine or ropivacaine be used over lidocaine?

A

Produce a much longer duration of action

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36
Q

Is ropivacaine or bupivacaine preferred and why?

A

Ropivacaine is preferred, because bupivacaine is severely cardiotoxic

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37
Q

What are the functions of the delta and kappa receptors? Which ones do most addictive opioids bind?

A

Mu receptor - site of beta-endorphin binding, also the target of most opioid drugs. (Mu-ssage)

Delta - site of enkephalin binding, mediate analgesia, but less so than mu receptors

Kappa - analgesia with psychotomimetic effects -> partial agonist drugs can bind this strongly

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38
Q

What is the mechanism of action once mu receptors are bound?

A

Think of the closed calcium ice cream cooler and the open barrel of bananas

Close voltage-gated calcium channels on the PREsynaptic membrane -> inhibit neurotransmitter release

Also open K+ channels -> hyperpolarization of nerve

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39
Q

What is Tramadol and what do its parent and daughter compounds do?

A

A synthetic codeine derivative - think of the tram in sketchy

Parent compound: SNRI - think of the N/S compass on the tram

Daughter compound: Codeine derivative which is active
-> weak Mu opioid agonist

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40
Q

What are the side effects of concern for tramodol?

A
  1. Increased frequency of seizures -> lowers the seizure threshold
  2. Serotonin syndrome - especially if used with MAOs.
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41
Q

What is dextromethorphan used for? Mechanism?

A

An isomer of a full-agonist opiate - little orphan cough drops

Used in combination with quinidine for chronic cough, as well as pseudobulbar affect

Also think of the NMDA camel -> has NMDA-antagonist activity as well (reason for abuse / robitussin)

Remember it is also a weak SNRI -> can precipitate serotonin syndrome like tramodol

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42
Q

How can opioids can elevations of serum amylase / lipase?

A

They cause sphincter of Oddi contraction as well (cause contraction of many things) -> reflux of bile / pancreatic enzymes

  • > think of the seagull sitting on the bile tree
  • > this can precipitate biliary colic
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43
Q

What are the partial agonist opioids?

A

nalBU-PHINe, BUtorPHanol, BUPRENorphine PENTAzocine

think of blue-phin bar (buprenorphine is also a partial agonist)

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44
Q

What is the mechanism of action of pentazocine?

A

Another mu partial agonist. Think PENTAzocine - cuz that’s how you learned it before apparently

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45
Q

How does naltrexone differ from naloxone?

A

Naltrexone has the same receptor blocking profile, but naloxone is used acutely for OD whereas naltrexone is used to prevent relapse, especially in once monthly injection (highly politicized treatment for opiate addicts)

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46
Q

What is the role of the cortex to suppress pain and how can neurotransmitter imbalance affect this?

A

Cortex sends down descending pathways which release NE, 5-HT, and GABA to facilitate the inhibition of excitatory pain impulses
-> pain loop should shut off overtime

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47
Q

What channels are modified to cause central sensitization?

A

In the descending axon which is normally inhibitory:

  1. Enhanced NMDA release on pain receptors and hence calcium influx
  2. Reduced GABA activity
  3. Reduced norepinephrine

Gained excitatory pathways and loss of inhibitory pathways -> enhanced central activation of pain pathways.

-> need to reverse this to stop neuropathic pain

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48
Q

What drugs block calcium channels in treatment of neuropathic pain?

A
  1. Gabapentin
  2. Pregabalin
  3. Topiramate
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49
Q

What drugs block sodium channels in the treatment of neuropathic pain?

A

Carbamazepine
Lidocaine
TCA’s -> also effective because they enhance NE / 5HT reuptake

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50
Q

How does peripheral sensitization occur?

A
  1. Inflammation damages or destroys peripheral nerves
  2. Threshold for firing is lowered, as regeneration of nerve triggers development of excess Na+ and adrenergic channels.
  3. Peripheral neurons fire impulses spontaneously leading to pain

to recap: Central sensitization involves sensitization of descending nerves, activating pain pathways. Peripheral sensitization involves the intrinsic firing of the nerve targeted by the central pathways.

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51
Q

What is central vs peripheral neuropathic pain and which are the most well studied?

A

Distinction made between where the lesion occurs, though a given syndrome may have components of both. Example of central neuropathic pain: MS, or post-stroke pain.

Peripheral - all the most well studied neuropathic pain, including:

  1. Post-herpetic neuralgia
  2. Diabetic neuropathy
  3. Trigeminal neuralgia
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52
Q

What water balance problem can SSRIs cause?

A

SIADH - think of the changing of the water cooler

-> especially true with fluoxetine

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53
Q

How do you differentiate NMS vs serotonin syndrome?

A

NMS - rigidity / hyporeflexia

Serotonin syndrome - clonus and hyperreflexia

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54
Q

What extra side effect do SNRIs have that SSRI’s do not?

A

Hypertension - due to increased norepinephrine

55
Q

What is the drug of choice for prophylaxis in tension headaches?

A

Amitriptyline - tricyclic antidepressant

Also useful in migraine prophylaxis
second line behind beta blockers and topiramate

56
Q

Which TCAs are known for having more or less anticholinergic effects?

A

Tertiary amines - i.e. AmiTRIptyline -> easier binds and inhibits the tertiary amine acetylcholine

Secondary amines - think north side prep secondary school -> Nortriptyline / desipramine have less cholinergic effects due to binding less tightly.

57
Q

What antiarrhythmic class are TCAs most similar to and why? What is the treatment in overdose?

A

Type 1A -> bind inactivated sodium channels to widen QRS, and ALSO prolong the QT interval

Treatment in overdose -> Sodium bicarbonate
Sodium -> restores Na+ gradient
Bicarbonate -> favors the unionized form of TCAs to prevent binding of inactivated sodium channels (they are amines so they are weak bases)

58
Q

What is the difference between MAO-A and MAO-B?

A

MAO-A - present in GI tract and liver, preferentially metabolizes 5-HT and NE, linked to depression. Also has some effect on DA (think of albino mouse chewing lower rope)
MAO-B - Preferentially metabolizes DA, think of black mouse chewing upper robe

Both will metabolize tyramine, but MAO-A inhibitors most important in GI tract (restrict diet here)

59
Q

What is the mechanism of action of tyramine similar to? What happens if it cannot be broken down

A

Similar to amphetamines - causes catecholamine release from nerve terminals

Found in aged cheeses / wines

  • > normally eaten by MAO-A albino mouses
  • > MAO inhibition (especiallyin GI tract) will precipitate absurd amounts of NE in the body -> hypertensive crisis
60
Q

What are the three most clinically important MAO inhibitors? What is their mechanism of action?

A
  1. Tranylcypromine - try a sip of wine
  2. Phenelzine - funnel leading into bottle of wine
  3. Isocarboxazid - box wine

They nonselectively bind and irreversibly inhibit MAO-A and MAO-B
-> must wait 2 weeks for regeneration before starting another serotonergic drug

61
Q

What is the only opiate which causes mydriasis and when must you also be careful when using it?

A

Meperidine (demerol)

  • > due to inhibition of NET/DAT
  • > also has weak serotonergic properties -> may precipitate serotonin syndrome when used with a MAO
62
Q

What medication class are doxepin and amoxapine in? What do other ones in this class end in?

A

Tricyclic antidepressants
-> these ones are mostly used in the treatment of insomnia due to strong H1 blockade

-Others end in -amine, tyline, or tiline

63
Q

What class is fluvoxamine in?

A

An SSRI with many CYP interactions

64
Q

Why does bupropion not have any sexual side effects? Is it useful in anxiety or any other conditions?

A

It is an NDRI, with no serotonergic effects which cause sexual dysfunction

Bad in anxiety -> can exacerbate

Useful in smoking cessation

65
Q

What is the mechanism of action of mirtazapine? Include all relevant receptors and their effects

A

Noradrenergic and specific serotonergic antagonist (NaSSA)

  • blocks 5-HT2 and 5-HT3 receptors (increases 5-HT1 agonism overall), with fewer sexual / GI side effects
  • blocks alpha2 receptors - increases NE in the synapse (increased sympathetic output -> think of mirth and misery sketch)
  • H1 antagonist - increases weight gain and sedation
66
Q

What is the mechanism of action of Vilazodone? What is its increased side effect?

A

SPARI - Serotonin partial agonist / reuptake inhibitor

SSRI + 5HT1A agonist -> possible increased efficacy for anxiety / depression

May make GI side effects worse

67
Q

What is the mechanism of action of trazodone?

A

SARI - Serotonin antagonist / reuptake inhibitor

  • SSRI plus antagonizes 52 - 5HT-2 receptors
  • also has anti alpha-1 (lighter) and anti-histamine (beeswatting on the bench) effects
68
Q

What is the usefulness of trazodone and its side effect profile?

A

Useful for insomnia due to anti-histamine effects

Alpha-1 blockade - can cause orthostatic hypotension (coach fainting)
Also causes priapism (erect trombone)

69
Q

What is the mechanism of action of Vortioxetine and why is it potentially better than other antidepressants?

A

SSRI + a number of agonist / antagonist effects (including 5HTT1, like Vilazodone and 5HT3 antagonism like Mirtazapine)

  • 5HT7 blockade my confer some advantage to patients with cognitive complaints over other SSRIs

Think Vilazodone + Mirtazapine serotonin effects + cognitive benefits

70
Q

Why might mirtazapine be useful in the treatment of the elderly or patients with depression + anorexia?

A

Histamine-blocking effect increases appetite -> stimulates weight gain

No sexual dysfunction

71
Q

Do mirtazapine / trazodone cause sexual dysfunction?

A

No, because serotonin agonism of the 5HT2 receptor is what’s responsible for sexual dysfunction
-> mirtazapine / trazodone both block these receptors

72
Q

Why does trazodone cause priapism and what other condition is known to precipitate this?

A

Alpha1 blockade -> vasodilation in the penis which cannot be reversed. -> reason why the condition is treated with intracorpeal epinephrine

Also caused by sickle cell disease -> sickling blocks venous outflow from penis

73
Q

What drugs are used to treat acute bipolar mania?

A

Atypical / typical antipsychotics
Carbamazepine - think of the car in the snow
Valproic Acid - Festival banner
Lithium

74
Q

What drugs / combinations are used to treat acute bipolar depression?

A

Atypical antipsychotic alone
Atypical antipsychotic / antidepressant combination (olanzapine / fluoxetine)
Lamotrigine - kid wearing llama suit on dad’s head
Lithium

75
Q

What drugs are used for maintenance treatment of bipolar?

A 
Atypical antipsychotics
Carbamazepine - mania / maintenance
Valproic Acid
Lamotrigine - depression / maintenance
Lithium
76
Q

What antiepileptic drugs are associated with SJS and why?

A

Phenytoin, carbamazepine, lamotrigine

  • > aromatic structure causes an abberant immune response to target self antigens
  • > especially in Asians with the HLA-B*1502 allele
77
Q

What antiepileptic drugs are most associated with weight gain and weight loss?

A

Weight gain - Valproate - think of the fat incan leader

Weight loss - Topiramate - think of the anorexic cannon boy near Toupee guy

78
Q

What is the mechanism of action of Topiramate and valproate?

A

Both are broad spectrum

Topiramate - Blocks Na+ channels, shaking hands with GABA = gaba agonist

Valproic acid - inhibits GABA deaminase (like vigabatrin), also blocks Na+

Basically they have the same MoA

79
Q

What are the side effects of topiramate?

A

Sedation - sleep soldier
Mental dulling / slowed cognition - confused soldier
Weight loss - cannon operator
Kidney stones - kidney shaped cannon wheels with cannonballs
Angle-closure glaucoma - they’re holding a literal eyeball tea kettle

80
Q

What are the major CYP inducers and inhibitors in the antiepileptic drugs?

A

Inducers - carbamazepine, phenobarbital, phenytoin

Inhibitors - Valproic acid

81
Q

What are the neurologic and reproductive side effects of phenytoin?

A

Neurologic: Diplopia, ataxia, sedation

Reproductive: Teratogen - most common is cleft lip and palate -> think of dude’s cleft baseball cap

82
Q

What are the dermatologic, musculoskeletal, and hematologic side effects of phenytoin?

A

Dermatologic: hirsutism (guy’s beard), gingival hyperplasia (blowing bubblegum), DRESS syndrome (waitress)

Musculoskeletal: Osteopenia (fracture axle, due to loss of Vitamin D via enzyme induction), SLE-like syndrome (lupus wolf)

Hematologic: Megaloblastic anemia (due to folate wasting, think of tossed salad)

83
Q

What are the important side effects of carbamazepine, and what does it do to the fetus?

A

Diplopia, ataxia
Agranulocytosis - hourglass
SIADH - ADH on guy’s head
SJS - especially in Asians with the HLA-B*1502 allele

Causes neural tube defects - like valproic acid. Think of exhaust pipe.

84
Q

What are the mechanisms of action of vigabatrin and tiagabine?

A

Vigabatrin - irreversibly inhibits GABA transaminase -removal of V-cab transmission

Tiagabine - GABA reuptake inhibitor - Tie stuck in V-cab (reuptake of the tie in inhibited)

85
Q

What seizures is carbamazepine ineffective against? Is phenytoin good for these?

A
  1. Absence seizures
  2. Juvenile myoclonic epilepsy

NO! Phenytoin is another narrow-spectrum agent

86
Q

What is one important consider in the dosing of phenytoin?

A

Undergoes zero-order (capacity-limited) metabolism when at therapeutic concentrations
-> much like alcohol / aspirin at higher doses

87
Q

Which anti-epileptic drugs are associated with a lupus-like syndrome?

A

Carbamazepine and phenytoin

-> think of the wolf in the middle of the picture

88
Q

What are the first line agents for neuropathic pain which isn’t trigeminal neuralgia?

A

Gabapentin, pregabalin (Ca+2 channel blockers), lidocaine patch (Na+ channel blocker), duloxetine (SNRIs)

89
Q

What are the second line agents for neuropathic pain?

A

tramadol, TCA’s, capsaicin (depletion of substance P)

90
Q

What are the high potency typical antipsychotics?

A

Think of the guy in sketchy flapping his wings on the roof “flying high”
FLUphenazine
TriFLUoperazine
Haloperidol

91
Q

What side effect is associated with thioridazine?

A

Irreversible pigmentation of reTina which may lead to blindness -> think of retina next to color theory wheel
-> may even look like retinitis pigmentosa

92
Q

What side effects are particularly associated with Chlorpromazine?

A

Photosensitivity + Corneal deposits

Chlorpromazine = Corneal
Thioridazine = reTinal
93
Q

How do high potency typical antipsychotics differ from low potency with respect to their side effects?

A

High potency - more D2 blockade, more likely to cause EPS / TD

Low Potency - more anti-M1,H1,and a1 effects, higher seizure risk / cardiotoxicity (QT prolongation)

94
Q

What are the extrapyramidal symptoms associated with D2 blockade? Describe them.

A
  1. Parkinsoninism - bradykinesia, cogwheel rigidity, masked facies, and RESTING tremor (resting on a park bench)
  2. Dystonia - abnormal muscle tone / spasm
  3. Akathisia - internal sense of restlessness
95
Q

How is akathisia treated?

A

Beta blockers, benzos, and anticholinergics (all EPS is treated with anticholinergics)

96
Q

How is drug-induced parkinsonism treated?

A

Benztropine - anticholinergic

-> don’t want to give D2 back as it will precipitate psychosis

97
Q

What features characterize neuroleptic malignant syndrome (NMS)? What labs go with it?

A

Life-threatening reaction to D2 antagonism

  • > Severe muscle rigidity (“Lead pipe rigidity”)
  • > Hyperthermia (guys face is bright red)
  • > autonomic instability - tachycardia, confusion, diaphoresis, labile blood pressure

Lab findings - Increased CPK and myoglobin due to rhabdomyolysis

More commonly precipitated by the 1st generation antipsychotics

98
Q

What are the treatments for NMS?

A
  1. Dantrolene - muscle relaxant blocking SR-mediated calcium release
  2. Bromocriptine - dopamine agonist
99
Q

How does the mechanism of action of typical vs atypical antipsychotics explain their efficacy in treating the symptoms of schizophrenia?

A

Typical antipsychotics - Strong D2 antagonists -> block dopamine increase in the nucleus accumbens / basal ganglia which mediates the positive symptoms of schizophrenia, while not helping the negative symptoms in the PFC where dopamine is low

Atypical antipsychotics - D2 and 5HT2A antagonists -> serotonin antagonism is thought to mediate improvement in negative symptoms as well

  • > salvador dali does NOT have a flat affect
  • > Think of the bite out of the serotonin happy face of cheese to remember the serotonin antagonism
100
Q

What three endings are common to atypical antipsychotics?

A
  • apine (olanzapine)
  • peridone (risperidone)
  • idone (ziprasidone = zipperazidone)
101
Q

What is the mechanism of action of aripiprazole?

A 
D2 partial agonist (blocks dopamine if there's alot)
5HT2A antagonism (accounts for effects)
5HT1A partial agonist -> like buspirone

More activating than other antipsychotics

102
Q

What atypical antipsychotic is considered like a borderline typical antipsychotic?

A

Becomes more like typical above 6mg daily -> EPS side effects

  • > due to more significant dopamine blockade
  • > think of the guy “whispering” (= risperidone) at the guy wearing the EPS newspaper hat + milk pouring out of his nose
103
Q

What atypical is associated with DRESS (drug reaction with eosinophilia and systemic syndromes)?

A

Ziprasidone (think of pretty lady with a zipper wearing a DRESS)

104
Q

What drug is most effective in treatment-resistant schizophrenia and its mechanism of action? How is it similar to lithium?

A

Clozapine

5HT2&raquo_space; D2 blockade

Similar to lithium by decreasing suicidality (perhaps due to frequent monitoring needed)

105
Q

What are the major side effects of concern for clozapine?

A

Agranulocytosis - shaking sandglass
Myocarditis - heart with a sandglass in it in sketchy
Seizures - shaking clock -> lowers seizure threshold
Anticholinergic effects - tea party painting behind clozapine closet

106
Q

What metabolic side effects are associated with atypical antipsychotics? What drugs in the class are most associated with this?

A

Weight gain and diabetes, dyslipidemia - stick of butter + candy in abstract art in sketchy

Olanzapine and clozapine

107
Q

What drugs are associated with increased chance of QT prolongation within the atypical antipsychotics?

A

All atypicals do, but especially Ziprasidone (zipper, next to the line dividers with QT prolongation strips in sketchy)

108
Q

What is the gold-standard treatment for Parkinson’s and how does it work?

A

Levodopa - L-DOPA rope

Carbidopa - Police car in the periphery in the scene

->carbidopa scares the L-Dopa guys in to bank vault (brain) by inhibiting L-Dopa conversion to dopamine peripherally (inhibits DDC - Dopa DeCarboxylase)

109
Q

What are the hallucinations which can happen with dopaminergic treatment and how can they be treated?

A

Usually visual hallucinations (because drug-induced), and they may become distressing

Treat with clozapine or quetiapine -> atypical antipsychotics less likely to block D2 and worsen symptoms

110
Q

What dopamine agonists are most commonly used for longterm management and which is not preferred? Why?

A

Preferred: Ropinirole (D2 agonist, two ropes), Pramipexole (pecs, D3 agonist)

Not preferred: Bromocriptine -> ergot alkaloid, partial agonism at alpha and serotonin receptors and causes more hallucinations

111
Q

What is apomorphine used for and what do you need to give with it?

A

Used for acute, rapid relief of “off periods”, but is a very potent trigger of area postrema and needs to be given with an antiemetic (non-D2, i.e. ondansetron)

112
Q

What is the role of COMT inhibitors in therapy?

A

They are used only as adjuncts to levodopa/carbidopa
-> smooth out the curve, have no role as a monotherapy

Remember the COMT as the interCOM guys which peripherally inactivate L-dopa (to 3-O-methyldopa)

113
Q

What are COMT inhibitors, how are they different, and what are their side effects of concern?

A

Tolcapone - Tall Al Capone - inhibits peripheral AND central breakdown of L-dopa and dopamine, but causes hepatic dysfunction (handle of gun)

Entacapone - Al Capone - stays in periphery blocking COMT, preferred agent with fewer side effects

114
Q

What is the role of MAO-B inhibitors in therapy? What are they and where do they act?

A

Can be used alone in early therapy, or as an adjunct to levodopa/carbidopa

Selegiline / Rasagiline - they act in the CNS (think of the black mouse eating the rope hanging from inside the bank vault)

115
Q

What is the first line treatment for early mild to moderate symptoms of Parkinson’s? What is the mechanism of action?

A

Amantadine - think of the manatees breaking the rope box open

  • > Increase dopamine release and decrease dopamine reuptake
  • > mild cholinergic antagonism
116
Q

What would be the side effects of levodopa given alone?

A

Nausea, vomiting - trigger of chemoreceptor trigger zone (dopamine agonism, reason why metoclopramide is used as an anti-emetic)
Hypotension - beta agonism
Cardiac arrhythmias

117
Q

What are the response fluctuations which can occur due to longterm levodopa/carbidopa?

A
  1. Peak dose dyskinesia - can occur 30 min after dosing due to huge CNS rush
  2. Wearing off - end of dose deterioration (bradykinesia / rigidity)
  3. On-off effect - random and unpredictable fluctuations occur with no relation to dosing
118
Q

What is one hard contraindication of dopamine therapy for Parkinsonism?

A

Any history of psychotic illness.

119
Q

What is the place in therapy of anticholinergic agents and which ones are used most commonly?

A

Think of the shaking car with three hexagons - Benztropine and Trihexyphenidyl

Best used for tremors > rigidity, does not help with bradykinesia - helps restore the cholinergic:dopamine ratio in the brain

120
Q

What is the firstline treatment for acute migraine?

A

Acetaminophen or NSAIDs + triptan (if severe)

Consider ergot alkaloids

121
Q

What are the first and second line suggestions for migraine prophylaxis?

A

First line: Beta blockers or topiramate

-Tricyclics like amitryptyline if h/o depression

Second line: Verapamil, if beta blockers not tolerated.
Valproic acid also an option

122
Q

What are the symptoms of cluster headache?

A

Unilateral headaches occurring repetitively in clusters of days to weeks

Sharp pain associated with autonomic symptoms
-> Lacrimation, rhinorrhea, periorbital swelling

123
Q

What is used for acute treatment and prophylaxis in cluster headache?

A

Acute - 100% oxygen therapy and sumatriptan (think of the cluser of lanterns above)

Prophylaxis - Verapamil preferred (makes no sense, cerebral vasodilation but a non-DHP)

124
Q

How exactly are triptans thought to combat migraine?

A

5HT-1B = Blood vessels, agonism causes vasoconstriction

5HT-1D = trigeminal nerve, agonism causes reduction of release of inflammatory vasodilators (i.e. Substance P, Calcitonin Gene-Related Peptide)

125
Q

Why is it important to treat headaches early?

A

The longer the neural activation and degranulation of inflammatory chemicals occurs, causing the vasodilation, the more “sensitized” the system becomes

-> need to rapidly terminate this cycle with triptans and an NSAID

126
Q

What causes a menstrual migraine?

A

Rapid changes in estrogen levels, which occurs especially before or during menstruation

Serotonergic systems are suppressed during late luteal phase (important in downregulating migraine) -> affects many women with migraine

Explains why migraines are more common in women

127
Q

What are the symptoms of cluster headache?

A

Unilateral headaches occurring repetitively in clusters of days to weeks

Sharp pain associated with autonomic symptoms
-> Lacrimation, rhinorrhea, periorbital swelling

Last 15-180 min, more common in men

128
Q

What is the mechanism of action of ergot alkaloids? What drug should be given with it?

A

Structurally related to monoamines, can cause potent vasoconstriction or dilation

  • > mechanism of action is sympathomimetic vasoconstriction of cranial arteries, or stimulation of 5HT-1 receptors
  • > very nonselective, dirty drugs

Give with metoclopramide -> prevents emesis from D2 agonism (drug is sympathomimetic, remember)

129
Q

What are the important contraindications of ergotamines?

A
  1. Peripheral vascular disease
  2. Renal impairment - may cause diversion of blood flow from kidneys
  3. Coronary artery disease -vasospasm
  4. Pregnancy (as mentioned early) -> placental vasospasm
  5. Concomitant triptan use
130
Q

Are triptans used to treat tension headaches?

A

No, they are thought to be just effective against cluster and migraine headaches.

Tension headaches should be treated with analgesic, NSAIDs, or acetaminophen

131
Q

What are the most serious adverse events of triptans and hence contraindications?

A

Coronary vasospasm -> MI, arrhythmias, and strokes

Contraindicated in Prinzmetal angina, coronary artery disease, and uncontrolled HTN

Avoid in hepatic disease (CYP metabolized). Don’t use with a MAO-A inhibitor within 2 weeks -> serotonin syndrome

132
Q

Which headache types are amitriptyline and verapamil used for again?

A

Amitriptyline - Migraine (if h/o depression, topiramate / beta blockers first line) and tension headache prophylaxis. Just remember TAM (Tension, Amitriptyline, Migraine).

Verapamil - Migraine and cluster headaches only

133
Q

What does having a very large arteriovenous concentration gradient mean about the onset of action for an inhaled anesthetic?

A

Large gradient = slow onset of action

This is because it means that peripheral tissues (the vast majority of the cardiac output) are uptaking the anesthetic very well, slowing the rate of rise of the overall anesthetic levels in blood. Full anesthesia cannot commence until the blood is saturated (largely dependent on there still being some anesthetic dissolved in the venous blood). This blood saturation is also dictated (obviously) by the blood:gas partition coefficient, with lower being better (less gas required to reach peak levels in blood). 
#660
134
Q

What are the symptoms of DRESS syndrome?

A

Exanthem-type morbilliform rash and fever, especially facial edema, with systemic symptoms like hepatitis, interstitial nephritis, arthralgias, lymphadenopathy, or hematologic abnormalities

Step 1 Miscellanous (40 decks)

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