-
3 physiological mechanisms of drugs to treat seizures
- 1. promote the inactivated state of voltage-activated Na channels
- 2. Enhance GABA
- 3. absence - limit activation of T-current, voltage sensitive Ca channel
-
5 off label uses of anti-convulsants
- migraines
- mood disorders
- schizo
- neuropathic pain
- neuromuscular disorders
-
most common seizure type and 4 causes
- partial
- cortex lesion
- tumor
- developmental malformation
- damage (stroke or trauma)
-
-
second most prevalent seizure and 2 causes
- generalized
- inheritance
- multiple mutant genes
-
pregnancy and anti-seizure meds
- 5% increase in stillbirth, mortality and birth defects
- metabolic epoxides and low epoxide hydrase activity
-
4 drugs for partial seizures
- carbamazepine
- clonazepam
- phenytoin
- valproic acid (adjunct)
-
2 drugs for absence seizures
-
3 drugs for grand mal seizures
- carbamazepine
- diazepam
- phenytoin
-
2 drugs for status epilepticus
-
4 stages of anesthesia
- 1. analgesia
- 2. delirium, excitation
- 3. surgical planes - muscle relaxation and respiratory depression
- 4. medullary paralysis, irreversible resp. depression and death
-
relief of preoperative anxiety, smooths induction through stage II to stage III and decreases airway resistance to the general agent
sedative-hypnotics
-
activity to dry up respiratory and salivary secretions
anticholinergics
-
provides sedation but additional protection against allergic reaction
antihistamines
-
relieve pre-op pain and provide complete anesthetic activity, smooths induction process
narcotic analgesics
-
2 MOA of GA's
- produce a certain partial pressure of the gas in brain tissue
- decrease neuronal activity by increasing the electrical threshol needed to induce an action potential
-
? affected in stage I
sensory pathways
-
? affected in stage II
inhibitory neurons
-
? affected in stage III
depression of the reticular activation system neurons
-
? affected in stage IV
CV and respiratory control neurons
-
miller-pauling theory
increased potency associated with the ability to induce ordered, crystal-like structure to water in neuron membranes
-
potency action of GA's
the ability of the agent to reduce surface tension - alter GABAA channels
-
what can be added to LA's to prolong tissue localization
epinephrine
-
all LA's have a high potential to cause ? and do what to combat
- allergic reactions
- co-administer an antihistamine (diphenhydramie or NO)
-
moa of LA's
prevents generation and conduction of action potentials and conduction by inhibiting ion fluxes, increasing the electrical excitation threshold. slow impulse generation and rise of the action potential
-
metab of ester's
degraded by esterases in the blood and tissue (1st pass effect)
-
metab of amide's
hepatically inactivated, finally the metabs are excreted renally
-
metab of muscle relaxants
- aproximately 50% excreted in the urine unchanged
- remainder demethylated hepatically
- followed by renal and biliary excretion
-
states that will prolong the duration of action of muscle relaxants
poor renal perfusion - shock or hypotension
-
MOA of cholinergic muscle stimulants
facilitate the transmission of impulses across the myoneural junction by inhibiting the destruction of acetylcholine by cholinesterase
-
pts to caution with cholinergic muscle stimulants
- bronchial asthma
- epilepsy
- peptic ulcer
- hyperthyroidism
- cardiac arrhythmias
- recent coronary occlusions
|
|