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PCL470 > Seizures (and a bit on anesthesia) > Flashcards

Seizures (and a bit on anesthesia) Flashcards

1
Q

Seizures

A

self-sustaining and self-limiting episodes of synchronized neural hyperactivity that can be detected by EEG

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2
Q

What causes seizures

A
  • brain trauma (head injury)
  • brain tumours
  • stroke, cardiovascular events
  • brain infection, meningitis, fever
  • medications (antidepressants, cocaine, amphetamine)
  • alcohol withdrawal
  • hormone fluctuations
  • hereditary forms of epilepsy
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3
Q

idiopathic epilepsy

A

idiopathic meaning unknown origin
- doctors now send DNA for testing to identify certain genes

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4
Q

EEG only detects

A

cortical activity (and in the gyri better than the sulci)

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5
Q

Thalamus is thought to mediate

A

really synchronized, slow-wave brain waves

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6
Q

Generalized seizures (absence and tonic clonic)

A
  • absence (petit mal): briefly unconscious, blank stare, no memory of the attack, lasts less than 30 seconds, 3 per second spike and wave throughout the whole brain.
  • tonic clonic (grand mal): unconscious, dramatic convulsions, no memory of attack, lasts less than 5 minutes, constant spiking throughout the whole brain
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7
Q

status epilepticus

A

grand mal seizing for over five minutes

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8
Q

Partial seizures (simple, complex)

A
  • simple partial seizure: conscious (a lot of cortex still working), has memory of the attack, sensory/motor/emotion symptoms, duration varies, localized spiking in neocortical or limbic area of brain
  • complex partial (temporal lobe): conscious but non-responsive, automatisms, no memory of attack, duration varies, localized then SPREADING spiking in one of both temporal lobes
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9
Q

Adverse consequences to not managing epilepsy

A
  • difficulty learning
  • breathing in food or saliva into lungs during seizure which can cause aspiration pneumonia (pulmonary pneumonias from lung infections)
  • injury from falls, bumps, self-inflicted bites, driving or operating machinery during a seizure
  • permanent brain damage (neurons irreplaceable)
  • death from seizures
  • death from suicide
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10
Q

epilepsy on a cellular level: calcium influx

A

Epilepsy is an imbalance of excitation
- results in seizure, head trauma, ischemic cell death

glutamate signalling results in:
- membrane depolarization > opening of voltage-gated calcium channels > influx of calcium
- NMDARs opening > influx of calcium
- Some GPCRs are linked to Gq > calcium release from store site

OVERALL, increase in intracellular calcium which leads to activation of Ca++ dependent enzymes and eventually, cell death

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11
Q

ion channels can be (choose your own adventure)

A
  • excitatory or inhibitory
  • ligand- or voltage-gated
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12
Q

therapeutic targets to reduce neuronal excitability

A

NT ion channels (ligand-gated)
- GABA (inhib)
- Glutamate and Acetylcholine (excitatory)
- not only regulated bu the levels or activity of the receptors, but also by the production, packaging, release, and clearance of NTs (so can target all those diff processes)

Voltage-gated ion channels
- sodium ion channels - propagation of the action potential
- potassium ion channels - repolarization/hyperpolarization of the membrane
- calcium channels - trigger the release of NTs

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13
Q

Four mechanisms of action for different anti-seizure medications

A
  1. Modulate voltage-dependent sodium channels (make them less active)
  2. facilitate GABA A channels and GABAergic transmission
  3. Negatively modulate voltage-gated calcium channels (calcium channel in thalamus thought to be important in absence seizures
  4. broad spectrum drugs with multiple targets
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14
Q

some epilepsy drugs that modulate voltage dependent sodium channels

A
  • phenytoin
  • carbamazapine
  • felbamate
  • lamotrigine
  • valproate
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15
Q

Epilepsy drugs that facilitate GABA a channels and GABAergic transmission

A

Agonists or positive allosteric modulator of GABA A
- agonist: topiramate
- Positive allosteric modulators: barbiturates and benzodiazedines
- block reuptake or metabolism of GABA: tiagabine, vigabatrin
- increase GABA synthesis: gabapentin, pregabalin

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16
Q

Epilepsy drugs that negatively modulate voltage gated calcium channels?

A
  • ethosuximide - inhibits VGCC in thalamus (T-type calcium channels)
  • gabapentin - blocks VGCC
  • lamotrigine
17
Q

Broad-spectrum target drugs for epilepsy

A

lamotrigine, zonisamide, topiramate, valproate

18
Q

Tiagabine

A

prevents reuptake of GABA into neuron

19
Q

Vigabatrin

A

blocks degradation of GABA

20
Q

Topiramate, phenobarbital, diazepam, lorazepam, clonazepam all have what in common?

A

act on the GABA A channel and promote its activation

21
Q

Gabapentin and pregabalin

A

both increase synthesis of GABA

22
Q

Epilepsy drugs that act at glutamate synapses

A

block VCSCs: phenytoin, carbamazepine, lamotrigine, felbamate

block VGCC: ethosuximide, lamotrigine, gabapentin

block post-synaptic AMPARs: phenobarbital, topiramate, lamotrigine

23
Q

What receptors do glutamate activate?

A
  • AMPARs (Na+ channe;s)
  • NMDARs (Na+/Ca2+ channels)
  • metabotropic receptors (mGluRs)
24
Q

What medication is used to treat absence seizures?

A

ethosuximide
- inhibits VGCC in the thalamus, T-type
- recall that the thalamus is thought to regulate the slow-wave synchronized sleep seen in sleep

25
Q

Contraindication of epilepsy meds

A

alcohol use

26
Q

phenytoin:
drug interactions

A

Can decrease the effectiveness of:
- oral contraceptives
- anticoagulants
- carbamazepine
- steroidal anti-inflammatory drugs

Potent inducer of cytochrome P450 enzymes so increases the metabolism of these drugs - can be an issue for drugs with a narrow therapeutic window

phenytoin pharmacokinetics can also be affected by multiple drugs - can be displaced from serum albumin

27
Q

phenobarbital:
drug interactions

A

Can decrease the effectiveness of:
- oral contraceptives
- anticoagulants
- carbamazepine
- and steroidal anti-inflammatory drugs

inducer of CYP 450 enzymes - increases metabolism of above drugs

28
Q

Valproate:
drug interactions

A
  • valproate increases serum levels of phenytoin
  • valproate and aspirin or warfarin can cause reduced clotting and spontaneous bleeding
29
Q

Common adverse effects of anti-seizure meds

A
  • somnolence: decreased activity of neurons in the reticular formation
  • GI upset: actions on autonomic nervous systems (depressed activity of cholinergic neurons innervating GI tract (parasympathetic nervous system)
  • cognitive impairment, memory problems: depressed activity of cortical neurons
  • physical dependence/withdrawal problems - CNS adapts to depressive actions of the anticonvulsant (if patient discontinues too rapidly, seizures may result)
30
Q

Purpose of anesthesia (3)

A
  1. immobility
    - spinal reflexes will cause twitching and large muscle jerks in response to cut
    - immobility / loss of reflexes is easy to measure and monitor for proper level of anesthesia
  2. amnesia
    - want to prevent explicit memory of surgery
    - also prevent implicit memory (info collected from sensory systems that does not reach conscious awareness - tested this with priming experiments)
  3. unconsciousness
    - prevent personal awareness. knock em out.
31
Q

Where does anesthesia act?

A
  1. immobilizing properties - neural inhibition at the spinal cord
  2. amnesic properties - hippocampus, amygdala, prefrontal cortex, sensory and motor cortex
  3. rendering patient unconscious - cortex, thalamus, reticular formation
32
Q

Anesthetics: administration

A
  • anesthetics can be inhaled or injected IV
  • inhaled anesthetics are easier to reverse and adjust dose
  • usually combo of IV and inhaled anesthetics is used
33
Q

Anesthetic drugs: injected and inhaled

A

injected:
- propofol, thiopental, diazepam, lorazepam, ketamine

inhaled:
- sevoflurane, desflurane, isoflurane (GABA agonists)
- halothane
- nitrous oxide

PCL470 (14 decks)

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