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86 Cards in this Set

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Antipsychotics (neuroleptics): what is another name for antipsychotics
neuroleptics
Antipsychotics (neuroleptics): name 4 antipsychotic drugs
thioridazine, haloperidol, fluphenazine, chlorpromazine (haloperidol +-'azine's)
Antipsychotics (neuroleptics): how do you keep benzos straight from antipsychotics
Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not perfect, but I'm working on it)
Antipsychotics (neuroleptics): what is the mechanism of most antipsychotics
block dopamine D2 receptors, anti-cholinergic, block alpha adrenergic receptors, block histamine receptors
Antipsychotics (neuroleptics): what is the clinical application of antipsychotics
schizophrenia, psychosis
Antipsychotics (neuroleptics): what are the side effects of antipsychotics
decrease of DA effects (off balance of DA and Ach where DA effects are decreased(bc of DA-antagonist) and effects of Ach are increased (bc the anti-Ach effects of drug are less than its anti-DA effects) causes extrapyramidal side effects: parkinsonian syndrome, akathisia (inner restlessness) , acute dystonic reactions, hyperprolactinemia (decrease of DA effects increases PRL release), muscarinic blockade (dry mouth, constipation), alpha blockade (hypotension), histamine blockade (sedation).
Antipsychotics (neuroleptics): what is a long-term effect of antipsychotic use
tardive dyskinesia (because of decrease of Ach effects. Long-term use of a DA-antagonist with anti-choinergics with decrease Ach effects causing huntington-like tardive dykinesia)
Antipsychotics (neuroleptics): what is neuroleptic malignant syndrome
a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia, hyperthermia. Use a DA agonist to trx (i.e. dantrolene)
Antipsychotics (neuroleptics): how do you treat neuroleptic malignant syndrome
dantrolene, dopamine agonists
Antipsychotics (neuroleptics): what is tardive dyskinesia
side effect of neuroleptics; stereotypic oral-facial movements, may be due to dopamine receptor sensitization
Antipsychotics (neuroleptics): what is the evolution of EPS side effects from antipsychotic drugs
evolution of EPS side effects: 4 hours -- acute dystonia (muscle spasm, stiffness, oculogyric crisis), 4 days -- akinesia (parkinsonian syndrome), 4 weeks -- akathisia (restlessness), 4 months -- tardvie dyskinesia
Antipsychotics (neuroleptics): is tardvie dyskinesia reversible
often irreversible
Antipsychotics (neuroleptics): what is fluphenazine used for
schizophrenia, psychosis
Atypical antipsychotics: name 3 atypical antipsychotics
clozapine, olanzapine, risperidone
Atypical antipsychotics: what type of antipsychotic is clozapine
atypical
Atypical antipsychotics: what type of antipsychotic is olanzapine
atypical
Atypical antipsychotics: what type of antipsychotic is risperidone
atypical
Atypical antipsychotics: what is the mechanism of atypical antipsychotics
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the mechanism of clozapine
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the mechanism of olanzapine
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the mechanism of risperidone
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the clinical application of clozapine
schizophrenia positive and negative symptoms
Atypical antipsychotics: what is the clinical application of olanzapine
schizophrenia positive and negative symptoms, OCD, anxiety disorder, depression
Atypical antipsychotics: what is the clinical application of risperidone
schizophrenia positive and negative symptoms
Atypical antipsychotics: how are atypical antipsychotics different from classic ones
atypicals treat positive and negative symptoms of schizophrenia, fewer extrapyramidal and anticholinergic side effects than classic antipsychotics
Atypical antipsychotics: which antipsychotics should be used to treat positive and negative symptoms of schizophrenia
atypical ones -- clozapine, olanzapine, risperidone
Atypical antipsychotics: which antipsychotics should be used for fewer side effects
atypical ones -- clozapine, olanzapine, risperidone
Atypical antipsychotics: what is a potential toxicity of clozapine
agranulocytosis
Atypical antipsychotics: which antipsychotic drug can cause agranulocytosis
clozapine
Atypical antipsychotics: what test must be done weekly on patients taking clozapine
WBC count because of potential agranulocytosis
Basic components of vision
visual acuity, contrast sensitivity, color, adaptation, periphersl vision, binocularity and stereopsis, central processing,
Principles and methods for functional assessment of vision
visual acuity (Snellen chart), contrast sensitivity (Pelli Robison- looks at how different lighting conditions can affect functional acuity), color (most screening tsts are for red-green colorblindness--- using CRT, color plates), adaptation (Process of adjustment to light changes), peripheral vision (tested with visual fields. affected people have a harder time to perceive a suden change, binocularity (use of both eyes) and stereopsis (depth perception) not needed for driving; tested by polarizing glasses or special examination devices., central processing
What is vision impairment and blindness
Blindness: 1. a person whose vision is insufficient to carryout normal sighted tasks (color blindness, night blindness), 2. a perso whose vision is restricted to 20/200 or worse in their better eye or with reduced central visual fields of less than 20 degrees. 3. a person with no vision at all ( no light perception--- rare)
Methods of evaluating the eye
Symptoms, function, appearance, diagnosticis, sturctural/anatomic (with slit lamp, fundus imaging), Elecrophysiologic.
Charles Bonnet phenomenon:
visual hallucinations inpeople with acquired blindness.
binocular aspects of vision: motor function, movement
Fixation on retina with microsaccades and drift allows scan of the visual field. Move fovea on the area of interest. ( the eye never really focuses on one point)
From eye to brain: optic disc and nerve
Visual processing: how we make sense of visual image.
CN3: which artery does it run parallel to? Which other fibers run with CN3 that are important to take notice of?
Posterior comm. Artery; pupillary fibers (PNS) on the medial surface.
Extraocular muscles and nerves: Describe the innervation of the extraocular muscles.
LR6SO4R3 : Lateral Rectus = CN VI, Superior Oblique = CN IV, and the Rest are CN III
Pupillary light reflex: List in sequence the nerves, brain structures, and muscles involved in the pupillary light reflex from illumination of one eye to bilateral pupillary constriction.
Light => retina => optic nerve => optic chiasm => optic tract => prectectal nuclei (synapse) => Edinger-Westphal nuclei (synapse) => oculomotor nerve => ciliary ganglion (synapse) => pupillary constrictor muscles
Internuclear ophthalmoplegia: What is the characteristic lesion in internuclear ophthalmoplegia?
destruction of the medial longitudinal fasciculus (MLF) => medial rectus palsy on attempted lateral gaze
Internuclear ophthalmoplegia: Name three characteristic clinical features of internuclear ophthalmoplegia.
1. On attempted lateral gaze, contralateral eye fails to abduct past midline; 2. Contralateral nystagmus on attempted lateral gaze; 3. Normal convergence
Internuclear ophthalmoplegia: What neurologic disease is commonly associated with internuclear ophthalmoplegia (aka MLF syndrome)?
multiple sclerosis; think MLF = MS
Visual field deficit with lesion: Name the visual field defect associated with a lesion of each of the following structures:
0
Visual field deficit with lesion: Right optic nerve
Right anopsia
Visual field deficit with lesion: Optic chiasm
Bitemporal hemianopsia
Visual field deficit with lesion: Rigth optic tract
Left homonymous hemianopsia
Visual field deficit with lesion: Right Meyer's loop (temporal lesion)
Left uper quadrantic anopsia
Visual field deficit with lesion: Right Meyer's loop (parietal lesion)
Left lower quadrantic anopsia
Visual field deficit with lesion: Dorsal optic radiation
Left hemianopsia with macular sparing
Where is CN 6 located? Damage to the nucleus leads to what condition?
Pons; ipsilateral gaze palsy
Where do saccades begin?
initiated by the superior colliculus of the midbrain and bordmann's area 8 aka frontal eye field
CN3: what conditions can damage CN3?
aneurysm fo PCA, uncus, when herniated through the tentroial notch, compression and inflammation of pupillary fibers
What is glutamate?
main excitatory NT
Glutamate: what are its 2 receptors?
AMPA and NMDA
Glutamate: What happens when it attaches to its receptors?
AMPA: Ca flows in; NMDA: Ca, and NA flows in
Glutamate: how is it cleard from synapses?
re-uptake via transporters on astrocytes
Glutamate: What happens when the NMDA receptor is over-activated?
Leads to excess calcium signaling that causes cell deathq
Glutamate: related drug development for Alzheimers
memantine- low affinity antagonist of NMDA glutamate receptor
Glutamate: What are glutamate uptake pumps on astrocytes dependent on?
Na/K ATP pumps.
Glutamate: What happen during a stroke (ischemia) to glutamate?
During oxygen deprivation, the glutamate uptake pumps are not able to work because there is no ATP being made from the Na/K pumps (which are oxygen dependent), thus glutamate remains in the synapse and overactivates the NMDA receptors leading to cell death.
Glial Cells: name 3 types
microglia, astrocytes, oligodendrytes.
What is the fxn of astrocytes?
k balance, take up glutamate/ GABA/ Glycine. Take up and metabolize glucose and provide nerve terminals with energy terminals with eneryg substrates (lactate). They also release factors that either constrict or dilate vessels
What is reactive gliosis?
the process of which astrocytes and microglia hypertrophy and proliferate and changing molecular expression/fxn after injury. Astrocytes changing their fxn could lead to high levels of TNFalpha which in turn increases AMPA recpetor expression on the ell surfact at synapses
what does microglia do?
it phagocytose cellular debris, recruits leukocytes and astrocytes via the release of chemokines, which my alter neuronal fxn. It regulates inflammation after CNS insult..
harmful effects of astrocytes after CNS injury?
failure of axon regeneration due to scar formation, neurotoxic substances are secreted (NO radicals)
T/F: Rehab training can lead to 'colonization' of neighboring cortex and undergo some reorganization anf "functional re-mapping" after a stroke
T
T/F surviving axon terminals can sprout "locally" when neighnoring terminals are lost
T
Auditory Systems: describe the pathway of the soundwaves right before it hits the tympanic membrane
sound waves converge through the pinna and outer ear to strike the tympanic membrane
Auditory Systems: after the sound wave strikes the tympanic membrane, how does it get transduced to electrical signals?
vibrations are transmitted by ossicles (malleus, incus, stapes) in the middle ear to the oval window and cochlea. Inside the cochlea are hair cells that transduces mechanical auditory stimuli into electrical signals that travel to the temporal lobe.
Auditory System: What is the auditory pathway from the cochlea to the brain?
electrical signals travel via CN8. CN8 has two branches: the cochlear branch, and the vestibular branch from the semicircular canals. The two branches join at the cerebellarpontine angle and then it travels up the dorsal and ventral cochlear nucleus. From the cochlear nucleus, it reaches the Superior olivary nucleus where it splits up to travel bilaterallly as the main auditory pathway called the lateral lemniscus. they then pass to the inferior colliculus then medial geniculate then to the auditory cortex.
Auditory System:does a unilateral hearing loss occur often? If it does occur, then what is usually indicative of?
no because the auditory fibers travel bilaterally. If it does occur, it is indicative of damage to the cochlear nucleus on the ipsilateral side or a sign of a lesion peripheral to the CNS
Inner ear: 3 components of bony labyrinth
cochlea, vestibul and semicircular canals
Inner ear: Site and composition of endolymph
membranous labyrinth, high potassium (like ICF)
Inner ear: site and composition of perilymph
bony labyrinth, high sodium (like ECF)
Inner ear: site of cochlear duct, utricle, saccule, and semicircular canals
membranous labyrinth
Inner ear: what frequency does base of cochlea pick up?
high-frequency
Inner ear: site and function of ampullae
in semicircular canals, for angular acceleration
Inner ear: site and function of maculae
in utricle and saccule, for linear acceleration
Inner ear: which frequency is lost first in hearing loss in elderly
high-frequency
Inner ear: site of endolymph production
stria vascularis
Inner ear: what part of the cochlea picks up low frequency sound?
the apex
Inner ear: if you have conductive hearing loss, which ear will the Weber test localize to? Is bone conduction or air conduction greater on Rinne testing?
Weber localizes to the affected ear. Bone conduction is greater than air conduction on Rinne
Inner ear: if you have sensorineural hearing loss, which ear will the Weber test localize to? Is bone conduction or air conduction greater on Rinne testing?
Weber localizes to the normal ear. air conduction is greater than bone conduction on Rinne
Antipsychotics (neuroleptics): what are its pharmacologic effects?
1. neuroleptic syndrome: psychomotor slowing, emotional quieting (sedation and tranquilization), sleepiness, restlessness, and emotional indifference. 2. Seizure threshold is lowered: Brain electrical activity slowed with increased synchronization. 3. inhibits vomitting: by blocking DA receptors in the chemotrigger zone. 4. Movement disorders: Alters DA neurotransmission in the basal ganglia 5. Hyperprolactinemia: by decreasing DA. Weight gain and increase appetite.