Neuro Flashcards
1
Q
what are seizures
A
- abnormal discharges of brain neurons
2
Q
where in the brain can seizures occur
A
- may occur in part (focal) or all (general) of the brain
- partial—one side
- general—both sides
3
Q
what is the difference between a simple and complex seizure
A
- level of consciousness
- simple: no loss of consciousness
- complex: loss of consciousness
4
Q
what is the objective of drug therapy with seizures and how do they work
A
- suppress seizures by maintaining an effective concentration of the drug in the blood and brain cells at all times
- effect ions used in impulses: Cl, Na, Ca
- choose a first-line antiepileptic agent specific to the seizure type
- cannot cure
5
Q
what are phenobarital and benzodiazepines and how do they work
A
- sedative/hypnotic drugs
- imitates the neurotransmitter GABA
- binds to GABA receptor
- opens chloride channel
- chloride rushes into the cell
- impulse stops
- more adverse effects with barbiturates than benzos
- lorazepam (or diazepam) intravenously (IV) = drug of choice in status epilepticus and in alcoholic-related seizures
6
Q
what are hydantoins and how do they work
A
- blocks sodium channels
- prevent sodium from entering brain cells
- message not started
- first-line therapy for partial (both simple and complex) seizures and generalized tonic-clonic seizures.
- teratogenic
- narrow therapeutic index (monitor blood levels).
- metabolized by P450 liver enzymes (CYP2C9)
- drug interactions with - metronidazole (increase phenytoin levels)
7
Q
what are some clinical guideline for patients taking hydantoins
A
- monitor for gingival enlargement
- monitor and emphasize oral hygiene; difficult for patient to adequately maintain oral hygiene because of tissue overgrowth
- place patient on frequent recall appointments to monitor gingival condition
8
Q
what is carbamezipine
A
- controls partial and generalized tonic-clonic seizures
- originally developed for the treatment of trigeminal neuralgia
9
Q
what are adverse effects of carbamazepine
A
- agranulocytosis (decreased white blood cells), platelet decrease, aplastic anemia.
- need medical consult for dental treatment.
- metabolized by CYP3A4 enzymes
- many drug interactions; erythromycin, clarithromycin, ciprofloxicin
10
Q
what are some guidelines for patients taking carbamazepine
A
- avoid erythromycin, clarithromycin (Biaxin), and doxycycline
- monitor for dry mouth
- monitor for blood disorders: infections, spontaneous bleeding (not provoked with an instrument), and poor healing
- look for oral ulcerations, dry mouth, and glossitis
- stress good oral hygiene
11
Q
what are other hydantoins
A
- valproic Acid (Depakene)/ - valproate (Depakote)
- metabolized by CYP2C9
- many adverse side effects.
- lamotrigine (Lamictal)
- used in children
- gabapentin (Neurontin)
- also used in chronic orofacial pain management
- not metabolized in the liver, so no drug interactions
- far safer than other drugs
12
Q
what are succinmides
A
- i.e. ethosuximide
- slow the entry of Ca into the nerve cell
- increases the threshold (cannot re-fire if busy firing)
- side effects: hiccups
13
Q
what is Parkinson’s disease
A
- age-related
- chronic, progressive, degenerative disorder of the CNS
- reduction in the neurotransmitter dopamine
- need balance of ACh and dopamine for control of normal muscle movement
14
Q
what are classic symptoms of Parkinson’s disease
A
- classic symptoms of Parkinsonism
- resting tremor
- muscle rigidity
- poker face
- bradykinesia (muscular movement becomes slow and rigid)
- masked facial expression
- “short step” walk
- postural instability
15
Q
what is the objective for treating Parkinson’s with drugs
A
- increasing the activity of DA (dopaminergic drugs) or decreasing the activity of ACh (anticholinergics)
- dopamine cannot get through the blood-brain barrier and get into the brain,
- give levodopa which then converts to dopamine in the brain
- combine levodopa with carbidopa (Sinemet) to reduce dose & SE of levodopa
16
Q
what is a dopamine replacement
A
- most effective during the first year of the disease; marked decrease in effectiveness by 3 years; by 5 years, signs and symptoms are back to the predrug level
- “on-off effect”
- fluctuations in response to levodopa
- increase involuntary orofacial muscle movements
- undergoes first-pass metabolism in the liver
- no dental drug-drug interactions
17
Q
what are dopamine agonists
A
- treating the “on-off effect” of levodopa
- prototype drug: bromocriptine (Parlodel), orthostatic hypotension
18
Q
what are anticholinergic agents
A
- early or mild stages of the disease or later on in combination with levodopa/carbidopa
- primarily effective for tremors
- prototype drug: benzotropine (Cogentin)
- adverse side effects: xerostomia
19
Q
what are monoamine oxidase B inhibitors
A
- selegiline (Eldepryl)
- rasagiline (Azilect)
- blocks the enzyme MAO-B, which metabolizes dopamine
- do not use Cipro when taking rasagiline
20
Q
what catechol-o-methyltransferase inhibitors
A
- newest class of drugs
- an adjunct to carbidopa-levodopa to help with motor complications due to levodopa
21
Q
what is the international classification of headache disorders
A
- primary headache disorders: migraine, tension-type, cluster headaches
- secondary headache disorders: identifiable cause i.e. sinus headache
22
Q
what is a rebound headache
A
- too much headache medication actually contributes to the headaches rather than easing them
- caffeine present in coffee and sodas and pain relievers may all contribute to rebound headaches
- don’t take pain relievers long-term
23
Q
what is a migraine
A
- 24 million people (18% of women, 6% of men)
- recurring, episodic and often severe headache disorder with attacks lasting 4 to 72 hours
- phonophobia (fear of sounds including your own voice), nausea, and vomiting, and cutaneous allodynia, aura
- one sided pain
- lights and sounds may aggravate
24
Q
what are the 2 phases of migraine attacks
A
- vasoconstriction: release of serotonin (5-HT), aura
- vasodilation: pain, substance P released
25
Q
what are the 2 goals of drug therapy for migraines
A
- two goals: abort current migraine or prevent migraine from occurring
1. abort (acute therapy): symptomatic therapy, either prescription or OTC. should not be used more than twice a week. more than twice a week or 4 times a month = preventative medications (chronic therapy) - therapy should start by eliminating all products containing caffeine, which causes vasoconstriction
- ID and eliminate triggers
26
Q
what are migraine drugs for relief
A
- serotonin agonists = triptans
stimulate 5-HT1 receptors (e.g., sumatriptan) - cause vasoconstriction
- analgesics (e.g., Excedrin, Tylenol Ultra) and nonsteroidal anti-inflammatory drugs (e.g., NSAIDs such as naproxen, ibuprofen)
- narcotics (Tylenol # 1, Tylenol # 3)
- ergot derivatives (dihydroergotamine = Migranal)
- cause vasoconstriction
27
Q
what are analgesics
A
- mild migraine attacks, analgesics alone or in combination with caffeine have been used
- NSAIDs
- naproxen
- overuse of analgesics and caffeine can aggravate the migraine (rebound headaches)
- use NSAID alone or in combo with triptan
- narcotic analgesics
- contain codeine
- preclude long-term use
28
Q
what are triptans
A
- orally administered triptans provide pain relief within 30 minutes
- injected sumatriptan has an onset of action in less than 15 minutes
- caution: blood pressure elevation
- caution should be used when using local anesthetics containing epinephrine
- patient’s blood pressure should be monitored
- caution when taken with SSRIs
29
Q
what are migraine drugs used in prevention
A
- beta-blockers (e.g., propanolol) - limit EPI use to 2 cartridges of 1:100,000
- drugs that inhibit sodium channels–antiepileptics or anticonvulsants (e.g., valproic acid) - xerostomia
- drugs that inhibit 5-HT reuptake into the nerve (e.g., tricyclic antidepressants such as amitriptyline) - lower dose than in depression; dry mouth; limit EPI to 2 cartridges of 1:100,000
- drugs that inhibit calcium channels and stabilize the blood vessels to prevent over dilating – CCB (e.g. verapamil)
