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83 Cards in this Set

  • Front
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Arousal

degree of sensory stimulation required to keep an individual at optimum level of cognitive function. Controlled by reticular activating system that extends from lower third of pons to thalamus.

Consciousness

state of awareness of self and environment. Made of two components: arousal and content (emotion and thought).

Sleep

active, recurrent, physiologic state that includes a reduction in consciousness and necessary fro health/well-being

Non-REM sleep

sleep stages N1, N2, N3 (slow-wave sleep).

REM sleep

Rapid eye movements, dreaming, increased respiratory rate/ body temp / blood flow / O2 consumption / penile erection. Muscle tone is absent. This type of sleep is not required but preferred.

Control of Wakefulness

locus ceruleus (NE), raphe nuclei (5-HT), tuberomammillary nucleus (H1), ventral periaqueductal gray matter (DA), some basal forebrain/brain stem (Ach), and hypocretinergic lateral hypothalamus

Control of Sleep

Reduction in neurons firing in wakeful centers, increase GABA firing

"sleep factors" that build up in the brain

adenosine, nitric oxide, prostaglandin D2.

Attention

cognitive function, focusing on relevant stimuli and ability to shift to other stimuli as they become relevant.

Delirium

Primarily due to a disorder of attention. Can have a disturbance of consciousness, decreased cognitive abilities, or hallucinations. Subacute onset.

Lesions in ________ areas can lead to delirium.

NE and ACh neurons in brain stem reticular activating system and basal forebrain.

Lethargy

abnormal state which the patient can be aroused with mild (non-noxious) stimulation

Stupor

abnormal state which the patient can be aroused with only vigorous/forceful/often noxious stimulation and still be cognitively impaired.

Coma

abnormal state which the patient cannot be aroused even with vigorous stimulation. Different from sleep in almost all ways.

Lesion in the basis pontis

Locked-in state. Normal consciousness but paralyzed, preservation of vertical eye movements

Diffuse cerebral cortical lesion

vegetative state. normal arousal and sleep cycles. No higher brain functions.

Bilateral medial frontal lesion.

Akinetic mutism. normal arousal and sleep cycles. Some higher brain function but inability to initiate thought, movement, and speech.

Lesions in these two areas can produce impaired consciousness (stupor or coma).

Reticular activating system or both cerebral hemispheres.

Focal supratentorial lesion with herniation

Decreased consciousness from "pressure dysfunction" causing pushing on the brain stem

Focal lesion of reticular activating system (diencephalon, midbrain, pons)

decreased consciousness, clinical picture of focal brain stem dysfunction that does not fit picture of cerebral transtentorial herniation.

Diffuse or multifocal lesion of bilateral cerebral hemispheres

Most common cause of impaired consciousness.

CNS depressant dose dependent degree of depression

Sedation --> sleep induction --> Loss of consciousness --> anesthesia --> Coma --> fatal depression

Difference between barbituates and benzodiazepines with regards to CNS depression.

Overdose with benzodiazepines does not cause fatal respiratory depression or coma while barbituates can.

Benzodiazepines

Enhance GABAa. Highly effecatious sedative hypnotic used for insomia. Can have psychomotor impairment, anterograde amnesia, tolerance, physical dependence, rebound insomnia.

Zolpidem

Novel benzodiazepine receptor agonists - bind to GABAa R. Most widely prescribed hypnotics - fewer deleterious effects.

Ramelteon

melatonin R (MT1 and MT2) agonist. Maintenance of circadian rhythm, help to initiate sleep. Far less efficacious than GABA acting drugs.

Suvorexant

orexin (hypocretin R antagonist). Used for tx of insomnia.

Barbituates

Bind to allosteric site on GABAa. Dangerous side effects lead to low use as sedative - hypnotics

diphenhydramine

first generation antihistamines (H1). May decrease sleep latency but not proven to increase total sleep. Residual daytime sedation, some anti muscarinic AE.

Drugs used for insomnia

Benzodiazepines, barbituates, ramelteon, suvorexant, diphenhydramine

MOA of drugs used for insomnia

enhance GABAa transmission, melatonin receptor agonists, H1 R antagonist

Stimulants

psychoactive drugs that temporarily improve mental/physical function. Can improve mood, reduce anxiety, lead to euphoria, stimulate respiration, suppress appetite.

Four most common stimulants

caffiene, theophylline, theobromine. Agonist activity at adenosine A1 and A2. Nicotine - nicotinic cholinergic receptors.

Amphetamine

taken up by DAT, NET, SERT and interferes with VMAT increasing catecholamine release. Increases arousal, decreased need for sleep, euphoria, psychosis. Tx: ADHD, narcolepsy

Methylphenidate

inhibits NET and DAT. Tx: ADHD, narcolepsy

atomoxetine

inhibits NET. Not a psychostimulant but increases alertness in ADHD.

Modafinil

psychostimulant inhibits both NET and DAT. Reduces sleepiness with low abuse potential. Tx: narcolepsy, shift-work sleep disorder, obstructive sleep apnea

Sodium oxybate (GBH)

CNS depressant, analog of GABA acting at GBH receptors. Improves quality of sleep. Tx: narcolepsy, severe cataplexy (transient attach of muscle weakness)

Drugs used to promote wakefulness

Modafinil, amphetamines, methylphenidate, sodium oxybate

Drugs used to promote attention

Stimulants (amphetamines, methylphenidate), nonstimulants (atomextine, buproprion, clonidine)

Desirable effects for anesthetic

induction of anterograde amnesia, skeletal muscle relaxation, inhibition of undesired autonomic reflexes, analgesia

Thiopental

Enhance GABAa, barbituate, IV general anesthetic

Propofol

Enhance GABAa, IV general anesthetic

Etomidate

Enhance GABAa, IV general anesthetic

Benzodiazepines

Enhance GABAa, IV adjuvant anesthetic drug to initially depress level of consciousness to produce amnesia or reduce anxiety

Fentanyl

mu opioid receptor agonist. IV Adjuvant anesthetic used for analgesia. Effects reversible by naloxone.

Ketamine

NMDA antagonist. IV Dissociative anesthetic - dissociates patient from environment.

Desflurane

Likely act at GABAa. Inhaled general anesthetic

Nitrous oxide

weak NMDA antagonist. Weak depressor of consiousness. Inhaled anesthetic.

Succinylcholine

Depolarizing neuromuscular blocking agent.

Vecuronium

Competitive inhibition of ACh receptors, neuromuscular blocking agent.

Typical pattern of brain hemispheric specialization

Left dominant for propositional language. Right dominant for nonverbal, spatial abilities. 30% chance of being reversed in left-handed or ambidextrous.

Left hemispheric control

propositional language, analyzing complex stimuli (details), analyzing temporal sequence

Right hemispheric control

Processing non-verbal/visuospatial information, synethesizing diverse parts into a whole (big picture), processing spatial information

Brocas area

inferior frontal gyrus (Left), controls muscle of speech and PRODUCTION of all forms of language

Wernickes area

superior termoral gyrus (Left), COMPREHENSION of all forms of language

Angular gyrus and supramarginal gyrus

Involved with reading and writing

Lesion in left hemisphere or thalamus

Aphasia - acquired disorder of language. Anomia - inability to name a recognized object

Lesion in angular gyrus or supramarginal gyrus

alexia - acquired disorder of reading. Differs from dyslexia which is a congenital reading disorder. May also have agraphia - acquired disorder of writing.

Lesion in Broca's area (inferior frontal gyrus)

Aphasia. Patient has slow, effortful speech, that is telegraphic. All other forms of output (writing, signing, foreign languages) are also affected. Comprehension is preserved.

Lesion in Wernickes area (superior temporal gyrus)

Aphasia. Speed of speaking normal but often uses wrong words or word-like sounds (paraphasic error). Often incomprehensible. Patient's comprehension of auditory and visual language is impaired

Lesion in the right hemisphere or parts of motor basal ganglia. Same disorder seen in Parkinson's disease.

Aprosodia. Speech lacking emotion of affection, loss of melody. Sounds like a robot.

Lesion in right cerebral hemisphere or right thalamus

Hemi-inattention. Neglect of left space. No visual field defects, but ignores everything perceived to be in their left field. May also have constructional apraxia - inability to put parts together into a whole

A lesion in the right or left cerebral hemispheres or thalamuses can cause this inability to copy drawings despite having comprehension of the task.

constructional apraxia

Bilateral lesion of occipital temporal visual system (sparing visual area)

Visual agnosia - inability to recognize objects despite normal visual acuity. Can recognize objects when presented auditory/tactile. Ex. patient can copy the image of a pig, will know its an animal, but cannot recognize the animal. If the patient hears "oink-oink" they know that's a pig.

Lesion of medial prefrontal lobe

difficulty initiating and sustaining motor acts. Appear apathetic / indifferent, decrease in spontaneity.

Lesion in orbital prefrontal lobe

socially disinhibited, ignore long-term needs, live in the present, unconcerned about pain/death

Lesion in dorsal prefrontal lobe

inability to deal in abstractions, difficulty changing strategies. Preservation - repetition of old behavior. Inability to plan for future.

Medial temporal lobe structures (hippocampal formation) important for memory

Parahippocampal gyrus, subiculum, hippocampus, dentate gyrus. All part of cerebral cortex.

Lesion in any of medial temporal lobe structures (usually diffuse)

basic amnesia syndrome - inability to learn new facts (short-term memory), retrograde amnesia, intact procedural memory, confabulation

Medial diencephalic structures

Mammillary nuclei, important for memory and dependent of vitamin B1

Lesion in left medial temporal lobe or left medial diencephalic structures

inability to form memories of verbal facts and events. (right sided lesions = inability to remember non-verbal facts/events)

Major cognitive disorder

significant cognitive decline in one or more domains, substantial impairment on cognitive testing, interference with independence in daily activities, cannot not be due to delirium or other mental disorder like depression.

Types of hallucinations

release hallucinations (spontaneous neuronal firing), due to neurochemical effects (5-HT2A, Anticholinergic, excess DA), dreams, ictal, from migraines, psychotic (schizoprenia, PTSD)

Delusions

firmly held false belief despite evidence to the contrary. Always psychotic. Can result from lesion or neurological disorder.

Psychosis

Loss of ability to determine what is reality. Secondary to neurological lesions in cerebral hemispheres or thalamus

Conversion symptoms

relatively persistent loss in sensory or motor function that cannot be explained by a physical disorder. Caused by "self-hypnosis"

Factitious disorder

patient intentionally falsifies or produces physical/psychological sx, but does not know why they are doing it. Muchausen syndrome is an extreme form where patients constantly hospitalize themselves.

Malingering

conscious faking of neurological or other illness, typically done for a specific purpose. Legal rather than medical problem.

Haloperidol

D2 receptor antagonist. First gen Antipsychotic. Decreases DA activity in mesocortical/mesolimbic pathways in the VTA.

Quetiapine and Aripiprazole

D2 antagonist + 5-HT2A antagonist. 2nd gen antipsychotic.

Donepezil

cholinesterase inhibitor. Tx: cognitive impairment from Alzheimers, only modest effect since impairment not solely from decrease in ACh in basal forebrain.

Memantine

low affinity NMDA R antagonist. Tx: cognitive impairment from Alzheimers, modest effect.