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Clinical Neuroscience 2 > Pharm- 15 > Flashcards

Pharm- 15 Flashcards

1
Q

What causes focal seizures to be focal?

A

Focal seizure, or partial seizure, is named for the focal nature (surprise) of where the brain is affected. Surround inhibition (same principle as eye inhibition) keeps the seizure location localized to one spot

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2
Q

How does focal seizures increase in strength to cause generalized seizurres?

A

GABA inhibition isnt strong enough

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3
Q

What i the key feature to distinguish focal seizures from generalized seizures?

A

The pt retains consciousness

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4
Q

What are the Sx to focal szrs in the frontal lobe?

A

a wave-like sensation in the head; in the temporal lobe, a feeling of déjà vu (glitch in the matrix)

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5
Q

What happens in a complex focal szr?

A

szr starts in 1 part –> spreads –> Sx’s spread accordingly.

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6
Q

What happens in secondary generalized szrs?

A

this type of seizure is bilateral due to spreading across the connections of the brain to the opposite hemisphere

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7
Q

What are the classical Sx of secondary generalized szrs?

A

loss of consciousness, and a tonic-clonic contraction of the body

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8
Q

What are the classical Sx of tonic-clonic (grand mal) szrs?

A

Loss of consciousness, and also as you would expect, intense contraction of both antagonist and agonist muscle groups.

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9
Q

What happens with the NMDA and AMPA receptors in the tonic phase?

A

They go super crazy

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10
Q

What happens to the AMPA and GABA receptors during the clonic phase?

A

They cycle back and forth,thats why u get jerky and spazzy

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11
Q

Where do absence szrs occur inth brain?

A

originate in a central location, and spreads to both hemispheres

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12
Q

What is the classical Sx of absence szrs?

A

characterized by a brief loss of consciousness

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13
Q

What is the mechanism to cause absence szrs?

A

T-type calcium channels, which are responsible for slow-wave sleep, so if they are activated, you just fall asleep right where you are. Somehow these calcium channels get activated inappropriately, leading to temporary loss of consciousness.

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14
Q

What are the 4 main mechanisms of anti-epileptic drugs (AEDs) to help wiht the Sx of szrs?

A

Drugs that increase Na+ channel inhibition
Drugs that inhibit calcium channels
Drugs that increase GABA mediated inhibition
Drugs that inhibit glutamate receptors

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15
Q

What is the mechanism to treat focal and general seizures?

A

treated via Na+ channel inactivation to stop channels, specifically channels that are cycling through open/closed states very quickly

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16
Q

What are the 4 drugs to treat local and secondary generalized seizures, which act on Na+ channels?

A

Phenytoin, Carbamazepine, Lamotrigine, and Valproic Acid

VPLC

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17
Q

What is the “use-dependent” mechanism of Phenytoin to treat szrs?

A

channels that are opened and closed at a high frequency, making them useless for slow, cyclical seizures such as Absence Seizures.

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18
Q

What % of phenytoin is bound to albumin in the blood?

A

95% bound to albumin

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19
Q

How is phenytoin metabolized in the body?

A

metabolized by the p450 hepatic system, and is an inducer of the p450 system (increases metabolism of fellow drugs metabolized by p450)

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20
Q

What is the T1/2 of phenytoin?

A

24 hour half life, because of its high albumin binding rate, if you give a patient too much, all of a sudden you may encounter very high levels of the drug in the plasma from virtually nothing before

21
Q

What drug is an inducer of phenytoin?

A

Carbamezapine

22
Q

What is an inhibitor of P450, causing the decreased metabolism of phenytoin?

A

Chloraamphenicol, Cimetidine, Disulfiram, Isoniazid

23
Q

Phenytoin increases the metabolism of which drugs?

A

Oral contraceptives, quinidine, doxycycline, cyclosporine, methadone, levodopa

24
Q

Why is carbamexapint pretty much the standard of choice for most patients that are also taking other drugs rather than phenytoin?

A

Linear metabolism

25
Q

Why can Lamotrigine treat absence szrs better than phenytoin/carbamezapine?

A

due to its ability to affect High voltage Calcium channels

26
Q

When do you use lacosamide?

A

Mechanism of action enhances slow inactivation of voltage gated sodium channels, and is another alternative to carbamazepine and phenytoin, especially for patients with drug-resistant epilepsy

27
Q

Which tpye of Ca channels does ethosuximide block?

A

T-type calcium channels

28
Q

What then does ethosuxamine treat>

A

absence szrs

29
Q

Which type of Ca channels does valproic acid target?

A

blocks both T-type and High voltage calcium channels

30
Q

Which Ca channels does gabapentin inhibit?

A

decreases release of excitatory neurotransmitter by inhibiting High Voltage calcium channels

31
Q

Which Ca channels does pregabalin treat?

A

blocks High Voltage calcium channels

32
Q

So in essence, blocking T-type Ca channels treats what type of szrs?

A

Petit mal (absence)

33
Q

And then blocking high voltage Ca channels treats what type of szrs?

A

Generalized

34
Q

What is the first line Tx drug for absence szrs?

A

ethosuxamide

35
Q

Valproic acid can increase GABA-mediated inhibiton by increasing which enzyme?

A

glutamic acid decarboxylase, the enzyme that synthesizes GABA

36
Q

Since valproic acid works on both T-type and high voltage-Ca channels, what types of szrs does it treeat?

A

Mixed

37
Q

Why is gabapentin weird?

A

the drug’s oral availability (giggity) is unpredictable

38
Q

Since pregabalin is more predictable than gabapentin, and inhibits high velocity Ca channels, what can it treat?

A

fibromyalgia and neuropathic pain

39
Q

Vigabatrin- mech of action

A

inhibits GABA metabolism, so it enhances GABA activity – blocks the enzyme GABA transaminase.

40
Q

Vigabeatrin- use

A

infantile spasms and refractory focal epilepsy

41
Q

Vigabentin- adverse reactions

A

induces metabolism of carbamazepine, bad effects may include peripheral visual field defects

42
Q

What are the main effects of benzos and barbs?

A

Benzodiazepines and barbiturates are GABA receptor helpers, and increase the effect GABA has on the receptors. They raise the action potential threshold by acting on GABA receptors, which open the Cl- channels

43
Q

What are the 4 benzos for szrs?

A

Diazepam, Lorazepam, Midazolam, and Clonazepam (pampampamapmapamama)

44
Q

Why is clonazepam unique, as far as what it targets?

A

it can inhibit T-type Calcium channels, helping stop absence seizures.

45
Q

What is the main mechanism of barbituates?

A

These work on all the different GABA receptors, and keeps the Cl- channel open longer than normal via allosteric binding as well as weak agonist binding to the GABA receptor. For the reason of weak agonist binding, it can actually enhance T-type calcium channels and help start absence seizures.

46
Q

What does phenobarbital treat?

A

partial seizures and tonic-clonic seizures

47
Q

Why is felbamate no longer used regularly to treat seizures?

A

Felbamate was found to be linked to fatal aplastic anemia and liver failure. It is now only used for patients with refractory epilepsy

48
Q

Rufinamide- mech of action

A

prolongs sodium channel inactivation, but it does so differently than the other drugs (phenytoin, carbamazepine) via a unknown MOA

49
Q

Rufinimide- use

A

No serious side effects, and can be used in place of felbamate for refractory epilepsy. Main treatments include focal seizures and drop attacks in Lennox-Gastaut syndrome (childhood onset of frequent/refractory seizures).

Clinical Neuroscience 2 (16 decks)

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