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Pharm Fall '24 > Test 3 - anticonvulsants (10/21) > Flashcards

Test 3 - anticonvulsants (10/21) Flashcards

1
Q

principle MOA of anti-seizure meds. (3)

A

1.modification of ion conductance (Na, K, Ca)

  1. enhancing inhibition (GABA)
  2. inhibiting excitation (glutamate)
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2
Q

Historical treatments of seizures

A
  1. Trephining (drilling into brain)
  2. cupping
  3. herbal remedies
  4. animal extracts
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3
Q

What causes seizures

A

Uncontrolled firing of CNS neurons

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4
Q

How much of the worlds population has seizures?

A

~1%

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5
Q

What are some of the causes of seizures?

A

variable
1. infection
2. neoplasm
3. head injury
4. heredity
5. toxic effects
6. metabolic disorder

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6
Q

Classification of seizures. what is the difference?

A
  1. focal - starts in small area of brain
  2. generalized - starts all over brain
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7
Q

What are the different focal seizures?

A
  1. simple focal
  2. complex focal
  3. Secondarily generalized
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8
Q

What do we see with simple focal seizures

A
  1. minimal spread of discharge
  2. don’t lose consciousness or awareness
  3. EEG may show normal discharge
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9
Q

What do we see with complex focal seizure. where do they arise from?

A
  1. affect level of consciousness
  2. may be unresponsive
  3. automatisms

-most arise from temporal lobes

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10
Q

What are the most common atiomatisms (5)

A
  1. lip smacking
  2. swallowing
  3. fumbling
  4. scratching
  5. walking about
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11
Q

what do we see with focal seizures secondarily generalized?

A
  1. begin as simple, but then spreads to rest of brain
  2. looks like generalized tonic-clonic
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12
Q

differentiate tonic and clonic

A

tonic- increased muscle tone all over body
clonic- rapid movement back and forth

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13
Q

What are the five generalized seizures?

A
  1. tonic clonic
  2. absence
  3. monoclonic
  4. atonic/tonic
  5. infantile spasms
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14
Q

What do we see with generalized tonic clonic seizures? what are the 3 phases?

A

-begin over entire surface of brain

  1. aura
  2. generalized tonic-clonic
  3. post-ictal
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15
Q

What do we see with absence (3)

A
  1. stare into space
  2. wake up, no notice of seizure
  3. some automatisms
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16
Q

What do we see with tonic seizures

A
  1. muscles contract and stiffen
  2. often falls down

Drop attack

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17
Q

what do we see with atonic seizures

A
  1. sudden loss of muscle tone
  2. fall without warning
  3. drop attack
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18
Q

What do we see with clonic and myoclonic

A

jerky mvmts

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19
Q

what do we see with infantile spasms (2)

A
  1. muscle spasms that affect childs head torso and limbs
  2. usually before age of 6 mo
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20
Q

Infantile seizures are indicative of ____

A

underlying pathology

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21
Q

Phenytoin is used for what seizures

A
  1. focal
  2. generalized tonic clonic
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22
Q

carbamazepine is used for what seizure type? What is it also used for? What kind of med is it?

A

Used for focal seizures.

Its a TCA (tricyclic antidepressant)

also used for trigeminal neuralgia and bipolar disorder

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23
Q

Pharmacokinetics for carbamazepine

A

D: increased protein binding (70% bound to plasma proteings)

M: induces hepatic enzymes

24
Q

True/false. Carbamazepine enhances metabolism of most other AEDs.

A

True

25
Q

Adverse effects with carbamazepine

A

diplopia and ataxia

26
Q

Lacosamide is used for what seizure

A

focal

27
Q

Phenobarbital is used for what kind of seizure

A

focal
generalized tonic clonic

28
Q

Lamotrigine is used for what seizure

A

focal and absence

29
Q

Ethosuximide is the drug of choice for what? what form does it come in?

A

absence.
can come in syrup form so good for kids

30
Q

valrpoic acid is used for what seizure

A

broad spectrum. Absence, bipolar, migraine

31
Q

What treatments can we use for infantile seizures

A

Often palliative. prednisone
GABA analog (keeps gaba around for longer period of time.)

32
Q

MOA for phenytoin

A

alters Na, K and Ca conductance.

33
Q

MOA for carbamazepine

A

blocks Na channel

34
Q

MOA for lacosamide

A

blocks Na channel

35
Q

MOA for phenobarbital

A

sedative-hypnotic

36
Q

MOA for lamotrigine (lamictal)

A

ion channel blocker

37
Q

uses for GABA analogs (vigabatrin)

A

adjunct, partial, neuralgia

38
Q

MOA for ethosuxamide

A

Ca channel inhibition

39
Q

MOA for valproic acid

A

Unknown but likely all.
-blocks high frequency firing
-effects on Na currents
-increase GABA
-increase K conductance

40
Q

MOA for benzo

A

increase GABA

41
Q

What do we worry about with phenytoin in regards to free form

A

it is highly protein bound so if we give a drug that completes for the binding site we can have more in the free form and it can be toxic in higher amounts

42
Q

Toxicity for phenytoin

A
  1. nystagmus
  2. Diplopia (double vision)
  3. Sedation
  4. gingival hyperplasia
  5. hirsuitism
43
Q

Pharmacokinetics of phenytoin

A

approaches zero order kinetics (see dosing, toxic levels)

44
Q

half life for carbamazepine

A

half life after one dose is 36hrs
half life after continuous therapy is 20hrs

45
Q

considerations for carbamazepine

A

inducer of cp450 (drug interactions)
compete for binding sites

46
Q

Lacosamide (vimpat) toxicity

A

dizziness, nausea, HA, diplopia

47
Q

phenobarbital toxicity

A

-sedation
-increase hepatic enzymes

Overdose
-respiratory depression

48
Q

What is the drug of choice for infant seizures?

A

Phenobarb

49
Q

What drug can actually worsen absence, drop, or infantile spasms

A

Phenobarb

50
Q

ethosuximide toxicity

A

-gastric distress
-lethragy

51
Q

valproic acid toxicity

A

-GI (N/V and heartburn)
-displaces phenytoin from proteins
-inhibits metabolism of other AEDs

52
Q

Phenytoin and valproic acid interactions

A

Phenytoin is highly protein bound and valproic acid can compete for that binding site and kick phenytoin off and we can have high levels of free phenytoin (no bueno)

53
Q

major considerations for status epilepticus

A

-life threatening emergency
-lasts at least 30min

-IV Benzo or fosphenytoin

54
Q

describe the half life and duration for diazepam

A

long half life (20-100hrs)

short duration (30min)

55
Q

Alternative therapies for seizures

A

craniotomy.
vagus nerve stimulation
keto diet

56
Q

What do we need before starting treatment for seizures

A

firm diagnosis to tell what kind of seizure. EEG or imaging

57
Q

anesthesia considerations during surgery of an epileptic patient

A
  1. adequate control during surgery
  2. phenytoin blocks NMB, higher levels can enhance.
  3. avoid methohexital, sevo, and demerol

Pharm Fall '24 (7 decks)

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