Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
35 Cards in this Set
- Front
- Back
atonic contractions
|
absence of postural muscle contraction
|
|
clonic contractions
|
(periodic symmetric body and extremity movements with regular amplitude and frequency),
|
|
myoclonic contractions
|
abrupt shock-like muscle contractions with an irregular amplitude and frequency)
|
|
Atonic seizures cause
|
a brief loss of motor tone (drop attack) that can cause falling
|
|
Generalized tonic-clonic seizures have an initial
|
tonic phase, which is associated with apnea and cyanosis, followed by a clonic phase where respirations become labored (5).
|
|
Partial seizures originate as
|
abnormal electrical discharges that are confined to a focal or restricted part of the cerebral cortex
|
|
Partial seizures are subdivided into
|
simple partial and complex partial
|
|
Two types of complex partial seizures that deserve mention are
|
temporal lobe seizures (characterized by a motionless stare and automatisms) and epilepsia partialis continua (characterized by persistent tonic-clonic movements of the facial and limb muscles on one side of the body).
|
|
New-onset seizures can be the result of a drug intoxication (e.g
|
., theophylline
|
|
Because of its prolonged effect is the initial agent of choice for treatment of convulsive seizures
|
, lorazepam
|
|
Intravenous phenytoin has been widely used to treat seizures since 1956. The standard intravenous dose is
|
20 mg/kg in adults
|
|
The combination of benzodiazepines and phenytoin will control seizures in 60–90% of cases of convulsive status epilepticus (11). In refractory cases, intravenous
|
phenobarbital can be effective when given in a dose of 50–75 mg/min until seizures are controlled or a maximum of 20 mg/kg is achieved. The therapeutic serum level for phenobarbital is 20 to 40 µg/mL.
|
|
The therapeutic serum level for phenobarbital is
|
20 to 40 µg/mL.
|
|
In addition to concurrent illness and surgery, several medications can precipitate or aggravate the myasthenic syndrome. The principle offenders are
|
antibiotics (e.g., aminoglycosides, ciprofloxacin), cardiac drugs (e.g., beta-adrenergic blockers, lidocaine, procainamide, quinidine), and magnesium (28). Magnesium blocks the presynaptic release of acetylcholine, and can be particularly detrimental in myasthenic patients.
|
|
In addition to concurrent illness and surgery, several medications can precipitate or aggravate the myasthenic syndrome. The principle offenders are
|
antibiotics (e.g., aminoglycosides, ciprofloxacin), cardiac drugs (e.g., beta-adrenergic blockers, lidocaine, procainamide, quinidine), and magnesium (28). Magnesium blocks the presynaptic release of acetylcholine, and can be particularly detrimental in myasthenic patients.
|
|
The first line of therapy in myasthenia gravis is
|
the administration of acetylcholinesterase inhibitors like pyridostigmine (Mestinon
|
|
The first line of therapy in myasthenia gravis is
|
the administration of acetylcholinesterase inhibitors like pyridostigmine (Mestinon
|
|
The first line of therapy in myasthenia gravis is
|
the administration of acetylcholinesterase inhibitors like pyridostigmine (Mestinon
|
|
Pyridostigmine can be given intravenously to treat myasthenic crisis (the IV dose is 1/30 of the oral dose) (27,29). Immunotherapy is added if needed using either
|
either prednisone (1–1.5 mg/kg/day), azathioprine (1 to 3 mg/kg/day), or cyclosporine (2.5 mg/kg twice per day) (
|
|
Pyridostigmine can be given intravenously to treat myasthenic crisis (the IV dose is 1/30 of the oral dose) (27,29). Immunotherapy is added if needed using either
|
either prednisone (1–1.5 mg/kg/day), azathioprine (1 to 3 mg/kg/day), or cyclosporine (2.5 mg/kg twice per day) (
|
|
Guillain-Barré Syndrome
|
some patients have circulating antibodies to gangliosides in peripheral nerv
|
|
the results of nerve conduction studies in GBS
|
slowing of nerve conduction due to demyelination
|
|
the results of nerve conduction studies in GBS
|
slowing of nerve conduction due to demyelination
|
|
the results of nerve conduction studies in GBS
|
slowing of nerve conduction due to demyelination
|
|
The treatment of Guillain-Barré syndrome mostly involves supportive care. In severe cases requiring mechanical ventilation,
|
plasmapheresis or intravenous immunoglobulin G (0.4 g/kg/day for 5 days) are equally effective in producing short-term improvement.Immunoglobulin G is often preferred because it is easiest to administer
|
|
Critical illness myopathy is observed in about one-third of patients with
|
status asthmaticus
|
|
Critical illness myopathy is observed in about one-third of patients with
|
status asthmaticus
|
|
Critical illness myopathy is observed in about one-third of patients with
|
status asthmaticus
|
|
Life-threatening increases in serum potassium can occur when what is given in the prescence of denervation injury?
|
Succinylcholine (Anectine)
|
|
Life-threatening increases in serum potassium can occur when what is given in the prescence of denervation injury?
|
Succinylcholine (Anectine)
|
|
gelastic seizures are associated with
|
Hypothalamic lesions (esp. Hamartomas)
|
|
gelastic seizures are actually
|
seizures that cause paraoxysms of laughter
|
|
gelastic seizures are actually
|
seizures that cause paraoxysms of laughter
|
|
gelastic seizures are actually
|
seizures that cause paraoxysms of laughter
|
|
gelastic seizures are actually
|
seizures that cause paraoxysms of laughter
|