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Pharmacology > Lecture 8: CNS > Flashcards

Lecture 8: CNS Flashcards

1
Q

What are the characteristics of a classic migraine?

A

Aura (may include any of the following: nausea, vomiting, visual scotomas, or even hemianopsia and speech abnormalities)

+

Severe throbbing/pulsing UNILATERAL headache for 1 hour to a few days.

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2
Q

What is the difference between a classic and a common migraine?

A

Common migraines do not have the aura.

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3
Q

What is the common treatment for migraines?

A

NSAIDs

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4
Q

What is the more pharmacologically advanced treatment for migraines?

A

Triptans

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5
Q

What is 5-HT?

A

Serotonin

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6
Q

What is 5-HT for?

A

Serotonin neurons are involved with mood, sleep, appetite, temperature regulation, perception of pain, BP, and vomiting.

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7
Q

What are the two 5-HT receptors we care about?

A

5-HT1B, which is the serotonin receptor found in the substantia nigra and globus pallidus (cheese of the pizza)

5-HT1D, general serotonin receptor in the brain.

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8
Q

What is the Mechanism of Action (MoA) for a triptan?

A

Act on intracranial blood vessels and peripheral sensory nerve endings, resulting in vasoCONSTRICTION and DECREASED release of inflammatory peptides.

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9
Q

What is the clinical indication for sumatriptan?

A

Migraines (First-line therapy for severe migraine attacks)

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10
Q

What are the contraindications for sumatriptan?

A

CAD
Angina (via coronary vasospasms)
Stroke
(Note: All are related to the vasoconstriction aspect)

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11
Q

If I need sumatriptan ASAP, what formulation should I take?

A

Injections or nasal

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12
Q

What is the first-line therapy for severe migraines?

A

Triptans

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13
Q

What are the other medications used for migraines besides triptans?

A

Ergot alkaloids, such as ergotamine

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14
Q

What is the MoA for ergotamine?

A

Vasoconstriction of smooth muscle working mostly at the alpha receptors.

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15
Q

What is the difference between ergotamine and sumatriptan?

A

Triptan is more effective for acute migraine attacks.

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16
Q

When is ergotamine most effective?

A

Very early in a migraine attack. Often combined with caffeine.

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17
Q

Why should I be wary using ergotamine and what are some side effects to be concerned about?

A

Frequent usage can cause rebound headaches.
Side effects can include Cyanosis, Ischemia, and prolonged vasospasms.

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18
Q

What are some prophylactic treatments for migraines?

A

None. (for acute migraines)
BUT
some common ones used still:
propranolol (non-selective BB and lipophilic), topiramate (anticonvulsant), and valproic acid (Anticonvulsant)

Uncommon: Amitriptyline (TCA)
verapamil (CCB)

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19
Q

How fast is sumatriptan’s onset?

A

1.5 hours orally, 0.2 hours SubQ.
This means I can take another one within 2 hours if I really need to.

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20
Q

What is chorea?

A

Chorea consists of unpredictable, irregular, involuntary muscle jerks that occur in different parts of the body and impair voluntary activity.

Huntington’s disease is also known as Huntington’s Chorea

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21
Q

What is athetosis?

A

Abnormal movements that are slow and writhing in nature.

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22
Q

What is dystonia?

A

Abnormal posturing

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23
Q

What are tics? Most notable disease?

A

Sudden, coordinated abnormal movements that occur repetitively. Usually in the head/face area, such as shoulder sniffing or sniffing in children.

Gilles de la Tourette syndrome or Tourette’s

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24
Q

What are some of the most notable signs of parkinson’s?

A

Combination of rigidity, bradykinesia, tremor, and postural instability. Bradykinesia often comes before the diagnosis can be made.

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25
Q

What is the pathology of Parkinson’s?

A

Loss of dopamine neurons in substantia nigra.
Dopamine normally inhibits GABA, which is an INHIBITORY NT.

Ach will bind to the GABAergic neuron to activate it, but dopamine normally inhibits it.

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26
Q

What are the two goals of treatment of Parkinson’s based on the pathophysiology?

A

Increase Dopamine levels.
Inhibit Ach.

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27
Q

What is the special characteristic of Levodopa vs dopamine?

A

Levodopa is a prodrug/metabolic precursor that CAN cross the BBB via an L-amine transporter (LAT). It is then decarboxylated.

Dopamine cannot actually cross the BBB, therefore injecting or eating dopamine does nothing for Parkinson’s

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28
Q

Why do we add carbidopa to levodopa?

A

Levodopa is decarboxylated by enzymes to dopamine. However, most of it gets metabolized too early in the peripheral bloodstream before it even reaches the brain.

Carbidopa is an inhibitor of the decarboxylating enzyme, so more Levodopa can get into the brain. Carbidopa DOES NOT penetrate to the BBB.

Concomitant adminstration of these two can reduce the daily amount of levodopa required by up to 75%.

29
Q

What are some common side effects of levodopa and carbidopa?

A

Dizziness, Nausea, dyskinesia, constipation.

30
Q

What does food do to levodopa?

A

Delays the appearance of levodopa in our bloodstream.

31
Q

What is the most common side effect of levodopa and how/why do we have issues treating it?

A

Dyskinesa, occuring in up to 80% of pts over a 10 year span of taking levodopa.

Development is dose-dependent and going off levodopa reduces the dyskinesia, BUT then the parkinson’s symptoms worsen.

We do not treat mild dyskinesia. We use amantadine (antiviral) to reduce more troublesome dyskinesia.

32
Q

If I have a patient having clinical fluctuations in their clinical response to levodopa due to the timing of their intake, what is this called?

A

Wearing-off reactions OR end-of-dose akinesia

33
Q

If I have a patient having fluctations in their clinical response to levodopa regardless of the timing of their intake, what is this called?

A

on-off phenomenon. This generally occurs in patients who responded to treatment well initially.

34
Q

What does on-off phenomenon present as clinically?

A

Off-periods of marked akinesia alternate over the course of a few hours with on-periods of improved mobility but often marked dyskinesia.

35
Q

What is a drug holiday for Parkinson’s and why/why not should I recommend it?

A

Discontinuance of a drug for 3-21 days.

MANY SIDE EFFECTS POSSIBLE: Aspiration pneumonia, venous thrombosis, pulmonary embolism, and depression resulting from immobility.

DO NOT RECOMMEND!

36
Q

What is pyrixidone (Vit B6) for?

A

Enhances extracerebral metabolism of levodopa, inhibiting its therapeutic effect.

37
Q

Why are MAO inhibitors a concern in a patient with Parkinson’s?

A

Combination of MAO inhibitors with Levodopa can cause hypertensive crises (via increased dopamine and/or NE).
Levodopa alone can already cause hypotension frequently or sometimes hypertension.

Always do a drug interaction check for any patient on a MAO inhibitor!

38
Q

What two things break down dopamine?

A

MAO-B
COMT

39
Q

How do COMT inhibitors work?

A

Prolong effects of Levodopa by diminishing its peripheral metabolism.

Decreases levodopa clearance and increases bioavailbility of levodopa.

40
Q

Why do we like COMT inhibitors?

A

Might help with patients receiving Levodopa who have response fluctuations.

Can help with smoother responses, prolonging on-time, and reducing daily dosage of Levodopa.

41
Q

Why do I use entacapone over tolcapone?

A

Tolcapone is associated with hepatotoxicity

42
Q

What is Stalevo and its effects/side effects?

A

Greater symptomatic benefit than just carbidopa+levodopa, but associated with earlier occurrence and increased frequency of dyskinesia.

43
Q

What is a seizure and what is epilepsy?

A

Seizures are finite episodes of brain dysfunction caused by abnormal discharge of cerebral neurons.

Epilepsy is a chronic disorder involving recurrent seizures.

44
Q

What are some common causes of seizures?

A

Infection, tumor, head trauma, hypocalcemia, degenerative diseases, genetic mutations, and epilepsy.

45
Q

What can cause neurons to be MORE excitable?

A

Increase in the intracellular flow of Na or Ca. Causes earlier depolarization.

OR

Increase in glutamate NT release. Glutamate is an excitatory NT.

46
Q

What can cause neurons to be LESS excitable?

A

Decrease in intracellular flow or Cl or efflux of K.

Decrease in release of inhibitory NTs like GABA.

47
Q

What are some clinical pearls?

A

Start low, go slow
When DCing a med, taper off slowly unless life-threatening toxicity.
The longer the therapy, the more extended the tapering should be. Write it out for patients!

48
Q

What are the two categories of seizures and their subtypes?

A

Generalized: Tonic, Clonic, Myoclonic, Atonic, and Absence

Partial/Focal: Simple (Without dyscognitive features), Complex (With dyscognitive features)

49
Q

What meds should be given for a tonic clonic seizure and what is a tonic clonic seizure?

A

Also known as a grand-mal seizure, characterized by muscle rigidity and jerking motions.

Carbamazepine, Lamotrigine, Levetiracetam (Keppra), Phenobarbital, Perampanel, Phenytoin, Topiramax (Topamax), and Valproic acid (Sodium valproate)

50
Q

What meds should be given for an Absence seizure?

A

Ethosuximide, valproic acid

51
Q

What meds should be given for a myoclonic seizure?

A

Lamotrigine & Levetiracetam (Keppra)

52
Q

What meds should be given for atonic seizures?

A

None that are FDA approved. Refer to non-pharmacological therapy.

53
Q

What is measured drug level inclusive of?

A

Both unbound and bound drug.

54
Q

What are Michaelis-Menten kinetics and what drug does it affect?

A

Phenytoin.

Michaelis-Menten kinetics means that a drug relies on a finite number of molecules that can metabolize it.
Phenytoin requires a certain transporter, which the blood does not have that many of. Once the amount of transporters is maxed out, the metabolism is maxed out.

55
Q

What is phenytoin subject to kinetic wise?

A

Michaelis-Menten kinetics
Protein Binding
Narrow therapeutic range

56
Q

What is an example of an auto-inducer drug and what does this mean?

A

Carbamazepine
It is both a substrate and inducer of 3A4.
Stabilizes with long-term therapy, but can induce its metabolism after 3-4 weeks.

57
Q

What are the 4 big inducers and what do they induce?

A

Carbamazepine: 2C9, 3A4, 1A2, and 2C19
Oxcarbazepine: 3A4
Phenobarbital: 2C9 & 3A4
Phenytoin: 2C9 & 3A4

58
Q

What is the one main inhibitor of 2C9?

A

Valproic acid/sodium valproate.

59
Q

What side effect categories are most antiseizure meds?

A

Category A: Sedative effects

60
Q

What are the two stimulant classes and which one is more effective at MAO inhibition?

A

Amphetamines and methylphenidates.
Amphetamines work better at MAO inhibition, also releasing catecholamines.

61
Q

What is the treatment protocol for ADHD?

A

Begin with a long-lasting stimulant of either class. If first trial fails, switch to a different formulation.
We typically start with methylphenidates (less effect on growth)
2nd failure would involve using a 3rd formulation or using a 2nd line non-stimulant.

Each trial should be 3 months.

62
Q

What is the PK of methylphenidates?

A

De-esterified prior to elimination, resulting in LESS metabolic drug interactions vs mixed amp salts.

Males usually have increased bioavailability.
Metabolized via 2D6. The bioavailability and half-life can be increased 4-8x greater via Bupropion (atypical anti-depressant)
Fluoxetine, and Paroxetine. (SSRIs)

63
Q

What is the difference in dosing timing for long acting and short acting stimulants?

A

Short acting is taken usually in the morning due to its quick onset. It can also be given in the evening.

Long-acting takes 60-90 minutes for onset, intended for once daily dosing, eaten only in the morning.

64
Q

What is the effect of food on stimulants?

A

Delays therapeutic effect by 30 mins -1 hr for IR
1-2 hrs for XR

Decreases bioavailability from 10-30%, even more so for beaded.

Capsule formulations can be sprinkled on semisolid food to help absorption.

65
Q

What are the common stimulant adverse effects and treatment options?

A

Reduced-appetite, weight loss (give high-calorie meal)
Stomachache (eat on a full stomach or lower dose)
Insomnia (take it earlier or sedate at bedtime)
Headache (divide dose, give analgesic)
Rebound (use long-acting, use antidepressant to inhibit)
Irritability/jittery (reduce dose or mood stabilizer or antipsychotic)

66
Q

What are the rare adverse effects for stimulants?

A

Dysphoria
Zombie-like state
Tics/abnormal movements
Hypertension/pulse fluctuations
Hallucinations

Reduce dosage or discontinue or change.

67
Q

What is the one kind of patient you should never give a stimulant to?

A

Schizophrenic patients.

68
Q

Which stimulant class has more pronounced effects on growth?

A

Amphetamines.

69
Q

What are the general adverse event classes for stimulants?

A

Psychosis/mania
Aggressive/violent behavior
Severe anxiety/panic attacks

Reduce or discontinue med.

Pharmacology (14 decks)

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