• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/151

Click to flip

151 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
What is the infectious agent associated with progressive multifocal leukoencephalopathy (PML)
Polyomavirus (JC) virus - infects oligodendrocytes causing demyelination
Usually seen in immunocompromised individuals
What is the infectious agent associated with subacute sclerosing panencephalitis (SSPE
Measles paramoyxovirus - infects oligodendrocytes causing demyelination
Describe anterograde amnesia, what is associated structure?
impaired new declarative memory, medial temporal lobe
Describe retrograde amnesia, what is associated structure?
Affects stored declarative memory, most recently stored memories most vulnerable.
Cortical and/or white matter damage
Describe short-term memory impairment, what is associated structure
Difficulty maintaining train of thought, prefrontal cortex/fronto-parietal connections
Example of a multiple memory system impairment
Example: Alzheimer's Disease, eventually affects both declarative and non-declarative memory
Conditions Associated with Parietal Damage:
Constructional Apraxia
Asomatognosia
Anosognosia
Constructional Apraxia: Inability to copy and object or put together parts of an object
Asomatognosia: denial that left side of body belongs to them (in right side attention dominant brain)
Anosognosia: denial of illness
How do you treat Alzheimer's disease
Cholinesterase inhibitors (Donepezil) - slows progression, but eventually trends downward
NDMA receptor antagonist (Memantine)
How to treat delirium
Correct underlying etiology
High potency antipsychotics help with agitation
Facilitate reality
NO benzos or anticholinergics
Etiologies for delirium
I WATCH DEATH
WHHHAM
Criteria for dementia dx
decline in memory with impairment in at least one other domain of cognitive reasoning
Criteria for delirium dx
Disturbance of consciousness with reduced ability to focus, sustain or shift attention
Differences between dementia and delirium
Delirium has marked psychomotor changes
Delirium has altered and fluctuating levels of consciousness
Delirium has short attention span
Differential dx for dementia
Delirium
Focal neurologic symptoms
Benign senescent forgetfulness
Medications/drugs
Depression
Clinical features of Alzheimer's disease (stages)
Stage 1 - memory disturbance, poor judgement, carelessness
Stage 2 - aphasia, apraxia, acalculia, worsening stage I, incontinence
Stage 3 - all cognitive functions affected, worsening stage II, motor disturbances
Gross findings of Alzheimer's disease
medial temporal atrophy w/ hydrocephalus
Gene mutations in familial Alzheimer's
Amyloid precursor protein, presensilin-1, presensilin-2

All have autosomal dominant inheritance
Presentation of fronto-temporal dementia (early to late)
Early presentation - behavioral changes associated with frontal lobe, speech and language related deficits (not memory)
Intermediate symptoms - anterior temporal lobe symptoms
Late symptoms - diminished attention, abstraction, problem solving, attention, Parkinsonism
Compare and contrast early presentation of Alzheimer's disease, Lewy-body dementia, and fronto-temporal dementia
AD - memory symptoms
FTD - behavior and speech symptoms
LBD - attention, visuospatial deficits, visual hallucinations
Dx criteria for fronto-temporal lobe dementia (FTD)
absence of plaques, tangles, and Lewy-bodes
Rule out other dementia causing diseases
Other causes for dementia (outside of FTD, AD, LBD)
Huntington's disease (autosomal dominant inheritance and Chorea)
Vascular dementia (ie. stroke)
Features of genetically linked Alzheimer's disease
Autosomal dominant
early onset (<60 years)
ApoE alleles are susceptibility factor for ____?
Alzheimer's disease
Dx criteria for dementia with Lewy-Bodies (DLB/LBD)

What is essential feature?
Fluctuating cognition with pronounced variations in attention and alertness
Recurrent visual hallucnations
Spontaneous Parkinsonism

Lewy-bodies are essential for dx
Infectious causes of dementia
HIV
neurosyphilis
Cryptococal meningitis
Whipple's disease
PML
SSPE
CJD
Microscopic findings in HIV associated dementia
microglial nodules commonly in white matter
Creutzfeldt-Jakob disease types
Familial
Sporadic
Variant
Iatrogenic
Clinical syndromes associated with sporadic CJD (early, late, end stage)
Early: nonspecific malaise, fatigue, deficits in appetite, sleep and concentration
Late: dementia and non-behavioral symptoms (motor symptoms
End stage: vegetative state, myoclonus, mutism, seizures, rigidity, autonomic dysfunction, hospital acquired infections
CSF and EEG findings in sCJD
14-3-3 protein in CSF
Periodic complexes in EEG
Imaging findings in sCJD
high signal in striatum, and least 2 cortical regions in diffusion-weighted imaging
Microscopic findings in sCJD
Neuronal loss, gliosis, NO INFLAMMATION/IMMUNE RESPONSE/VIRAL SYMPTOMS

Microvacuolation - all layers o cortex
Differences between sCJD and vCJD
Younger patients compared to sCJD
Longer duration of illness than sCJD
No abnormal EEG in vCJD
14-3-3 in only 50% of vCJD cases
Earlier psychiatric and sensory symptoms in vCJD
Examples of tauopathies
FTDP17 (frontal-temporal dementia w/ Parkinsonism linked to chromosome 17)
Pick's disease
Examples of synucleinopathies
Lewy body dementia (diffuse Lew bodies)
Parkinson's disease (only brainstem Lewy bodies)
Describe the two types of Lewy bodies
Classical (brainstem): eosinophilic w/ halo, multiple in one cell

Cortical: small neurons in layers V, VI, no halo
Describe etiology of Wernicke's encephalopathy
Thiamine (B1) deficiency
Clinical presentations of Wernicke's encephalopathy
Anterograde amnesia, confabulations, loss of medial dorsal nucleus of thalamus

Slight retrograde amnesia
Gross findings of Pick's disease
Atrophy (<1000 gms), fronto-temporal lobar atrophy, asymmetric atrophy, knife edge atrophy
Where are NFTs found in AD
Paired helical filaments in neocortex, hippocampus, amygdala, basal forebrain nuclei
Composition of NFTs
Tau, ubiquitin, amyloid-Beta
Where and what are neuritic plaques in AD?
neocortex, hippocampus, amygdala, basal forebrain nuclei (same as NFTs)

expanded dendrites (dystrophic neurites), mitochondria, central amyloid-Beta core
What is CERAD?
Measurement of plaque density per age and history to establish AD dx
What are the micro findings of FTDP17
Accumulation of soluble and insoluble TAU in neurons and/or glia

NO amyloid deposits or other disease specific abnormalities
Micropathological findings of Pick's disease
Neuronal loss and gliosis of outer cortex, caudate, thalamus, sparing of glboal pallidus

Presence of Pick bodies
Where and what are Pick bodies
Introcytoplasmic inclusion

Found in dentate gyrus,amygdala, septal nuclei, cortex

Consist of Tau and a-synuclein
Microscopic findings of Lewy body diseases
Stain with ubiquitin and a-nuclein, but NOT tau

cortical microvacuolation but not to extent of CJD
What mutation is associated with prion diseases
PNRP gene on chromosome 20
What enzymes are present in normal APP processing?
1) alpha-secretase
2) gamma-secretase
What enzymes are present in abnormal APP processing? What is formed?
1) beta-secretase
2) gamma secretase

Forms amyloid-beta-42 segments (prone to aggregation)
Describe role of presensilins, what happens when mutations occur?
Interact with gamma-secretase
What is the clinical triad of Wernicke's encephalopathy?
Delirium, ataxia of gait, eye movement deficits with nystagmus
What is the clinical triad of normal pressure of hydrocephalus?
Dementia, gait disturbance, urinary incontinence

No mass effect or blockage
Who is most at risk for Wernicke's encephalopathy?
Malnourished alcoholics
What causes Korsakoff syndrome?
untreated thiamine deficiency (Wernicke's encephalopathy)
Understanding agent, host and environment in drug abuse
Agent - drug itself (availability, effects, cost)
Host - user (hereditary, metabolism, co-morbidities, etc.)
Environment - social setting, peer influence, conditioned stimuli, etc.
What is the Kindling model?
Overlapping neurobiological pathways, repeated disruptions of brain functions sensitizes neurons that contribute to other disorders
What is physical dependance?
Altered physiological state produced by repeated drug use necessitating continuation to avoid withdrawal
What is innate tolerance?
Genetically determined sensitivity to a drug that is observed in naive user
What are the types of acquired tolerance?
Metabolic (pharmacokinetic) - increase in metabolism leading to less drug at receptor

Functional (pharmacodynamic) - less action at receptor despite same amount of drug

Learned - reduced effects due to compensatory mechanisms and behaviors
What are 3 withdrawal techniques?
Cross dependence - suppress physical dependence on drug with agonist (reinforcement)

Antagonist withdrawal - block reinforcing effects of drug with antagonist (extinction)

Aversive withdrawal - induce negative effects when drug is administered (positive punishment)
Describe the ischemia cascade
Ischemia --> Ca influx --> excitatory NTs, lactic acidosis --> free radical formation, NO release
What is the rationale for hyperacute therapy of stroke?
Preserve viable penumbra tissue
How is blood flow restored during hyperacute therapy for stroke?
T-PA thrombolytic
What are the indications for T-PA use?
Within 3 hours after onset of stroke (potentially effective after 4.5 hours)
What is the recommended treatment for blood flow restoration after T-PA window has passed?
Intra-arterial or mechanical thrombolysis
What is the recommended evaluation and workup for ischemia stroke?
Assessment
Imaging
CTA/MRA
Echocardiogram
BMP, CBC/diff/coagulation
fasting lipid
thyroid
EKG
CXR
What is the mechanism of T-PA?
Catalyzes conversion of plasminogen toplasmin
Drugs used for anti-platelet Rx
Aspirin
Dipyridamole
Thienopyridines
Drugs used for anti-coagulant Rx
LMW heparin
Warfarin
Dobigatran
Rivaroxaban
Indications for anti-coagulant RX
Secondary prevention of cardiogenic stroke and primary prevention of stroke in A-fib

Do not use in patients within 24 hours of T-PA
Acute therapy for ischemic stroke
Lower blood pressure over time
Antithrombotic RX (unless T-PA was used
Protect airway
Treat hyperglycemia
DVT prophylaxis
Treat fever or seizures
Start PT/OT/ST early
How to treat intracranial hemorrhage
Antihypertensive RX
Metabolic vs. structural coma
Delirium more common in metabolic
Global deficits more common in metabolic
Posturing less common with metabolic
Eye reflex remain in metabolic
Asterixis and myoclonus in metabolic
From where does the hippocampus formation receive it's inputs?
Entorhinal cortex
Parahippocampal cortex
Piriform cortex - receives input from olfactory bulb
What structures make up the hippocampal formation?
Hippocampus proper
Dentate
Subiculum
Trace the hippocampal loop
Cell bodies from entorhinal cortex --> dentate gyrus --> CA3 --> 2 branches
Trace the two branches of the hippocampal loop
branch I (from CA3) --> CA1 --> subiculum --> entorhinal cortex

branch II (from CA3) --> papez loop
Trace the Papez loop
fibers from CA3 --> form fimbria and create fornix --> mammilary bodies --> anterior nucleus of thalamus --> cingulate cortex --> entorhinal cortex
What are the amygdala's functions?
Emotional memory and learning

- associated learning (fear conditioning)
- appetite conditioning (addiction)
- modulation of explicit memory (attaching emotional meaning to stimuli)
Describe the 3 loops of the amygdala
Emotion loop - receives inputs and communicates with cingulate cortex and N.A.

Endocrine/autonomic loop - regulates septal basal forbrain

Olfactory loop - similar to piriform-olfactory pathway
What occurs in patients with lesions in the amygdala?
Tame placid behavior
Friendliness
Inability to recognize emotion from facial expressions
What part of the brain is involved in attention guidance?
Posterior parietal cortex - main one

Prefrontal cortex

Subcortical structures (superior colliculus, Pulvinar nucleus of the thalamus)
Where is the source of norepinephrine? And where do these sources project?
Local coeruleus --> forebrain

Lateral tegmental area --> subcortical structures
What is the role of acetylcholine in the higher cortical functions?
Boost signal to noise ratio, arousal and attention
What is the source of aceytlcholine?
Basal forebrain --> septal nuclei, diagonal band of Broca, nucleus basalis

Pedunculopontine nucleus, dorsal tegmental nucleus --> subcortical structures
What is the role of domapine in higher cortical functions?
Euphoria system
What is the source of domapine and it's targets
Ventral tegmental areas, substantia nigra --> frontal cortex, striatum, limbic system
What is the role of serotonin
Mood regulation
What are the sources of serotonin?
Midbrain raphe --> forebrain
Pontine, medulla raphe --> subcortical structures
What area of the brain controls functions such as restraint, judgement, initiative and order?
Prefrontal cortex
What RX is indicated for opiate addiction?
Methadone
Buprenorphine - partial mu agonist
Maltrexone - mu antagonist for OD
Opiates exhibit what type of tolerance?
pharmacodynamic tolerance
Alcohol exhibits what type of tolerance?
pharmacodynamic and kinetic
What RX is indicated for alcohol addiction?
benzodiazepines (diazepam) - for withdrawal seizures
Carbamazepine - for withdrawal seizures

Disulfiram - blocks metabolism
Naltrexone - mu antagonist
Acamprosate- NDMA antagonist
What type of tolerance is exhibited by barbituates?
Pharmacodynamic and kinetic
Why is overdose common with benzodiazepines?
Tolerance develops to many effects except for lethality
What type of tolerance is exhibited by benzodiazepines?
Pharmacodynamic
What RX indicated for benzodiazepine or barbituate addiction?
Carbamazepine or phenobaritol (long half life)

Flumazenil for overdose
What RX is indicated for nicotine addiction?
nicotine replacement therapy
Buproprion - sustained release antidepressent
Varenicline - partial nicotinic agonist
What is the mechanism for cocaine and amphetamines?
Dopamine reuptake block
Benzoylecgonine is found in urine after use of what drug?
Cocaine and amphetamines
What RX is indicated for stimulant addiction?
Symtptom RX

Modafinil - for narcolepsy
Disulfiram - unkonwn mechanism
What is the endogenous cannabinoid ligand?
anadamide
Describe the difference between functional and ischemic hypoxia
functional - low pO2, low O2 carrying capacity, inhibition of O2 use by tissue

Ischemia - low blood flow
What causes global cerebral ischemia?
Systemic hypotension
Cardiac arrest
What causes focal cerebral ischemia?
Large vessel occlusion - fixed occulsions (thrombosis), embolus

Small vessel occlusion - arteriolosclerosis (lacunar infarct)
What regions of the brain are most sensitive to global ischemia?
CA1 - hippocampus
Cerebellum
Cortical neurons in layers 3 and 5
What are some etiologies for large vessel occlusion cerebral ischemia?
Thrombosis
Atherolosclerosis
Vasculitis
Hypercoagulation
Dissecting aneurysm
Drugs
CADASIL
Why do watershed infarcts commonly include hemorrhage?
Watershed infarcts are usually caused by systemic hypotension, hemorrhage occurs when re-perfusion occurs
What is laminar necrosis?
Deep cortical necrosis in watershed regions with scarring due to microglial insult
What is most common cause of a bland infarct?
Embolism
What are the most common causes of emboli to the brain?
Vegetation on valves from infections
Cardiac mural thrombus (from M.I.)
Carotid plaques
Were are lacunar infarcts typically found?
Tissues perfused by penetrating small vessels
What is the most common cause of subarachnoid hemorrhage?
Saccular aneurysms - dissection can lead to sudden death
What conditions are associated with venous sinus thrombosis
Bilateral hemorrhagic infarcts
What are some etiologies of intracerebral hemorrhage?
Arteriolosclerosis
Hypertension
Coagulopathy
Vascular malformations
Aneurysms
Neoplasm
Drug use (cocaine, ampethamines)
What are some "organic" etiologies for a patient with psychotic symptoms?
Trauma
Infection
Organ failure
Brain lesions
Drugs or toxins
What are some psychiatric etiologies for psychosis
Delusional disorders
Mood disorders
Cognitive disorders
CD
Dissociative disorder
Personality disorder
Schizophreniform
what are positive symptoms of schizophrenia?
Hallucinations in all sensory modalities
Delusions
Thought disorders (disorganized speech, cognitive impairment)
What are negative symptoms of schizophrenia?
Ahedonia-asociality
Inattentiveness
Affective flattening (lack of expression)
Alogia (thought blocking)
Apathy
What are the 3 phases of schizophrenia?
Prodrome
Active phase
Residual phase
What symptoms are most prevalent in active phase schizophrenia?
Positive schizophrenic symptoms (hallucinations, delusions, etc.)
What symptoms are most prevalent in residual phase schizophrenia?
Negative schizophrenic symptoms (social withdrawal,
Describe the first rank symptom for schizophrenia
Complete auditory hallucination - when sounds are heard from outside your head
DSM-IV criteria for schizophrenia includes
At least two of the following:
delusions
hallucinations
disorganized speech
disorganized behavior
negative symptoms
What are the subtypes of schizophrenia?
paranoid
disorganized
catatonic
residual
undifferentiated
What RX is indicated for schizophrenia?
Hospitalization for safety and monitoring
Antipsychotic medication
Psychosocial rx
How is white matter volume correlated with schizophrenic symptoms?
Complete auditory hallucination is correlated with less white matter volume

Internal hallucinations is correlated with more white matter volume
What commonly mimics schizophrenia?
Schizotypal personality (Cluster A disorders)
What are the two models of sleep-wake regulation?
Homeostatic (sleep load) - the more you're awake the sleepier you get

Circadian alert signal - histamine keeps you awake
What is the mechanism of sleeping pills?
pro-GABA release to inhibit histamine
What structures localize sound?
Medial superior olive - time delay
Lateral superior olive - level differences
Explain connections of olivocochlear efferent system
lateral superior olive - connects to IHC

medial superior olive connects to OHC
What are the functions of different GABA-a receptor classes?
alpha-2 - anxiety
alpha-1 - sedation
alpha-5 - learning and memory
Treatment for alcohol abuse
disulfiram - blocks acetaldehyde metabolism and causes severe withdrawal

acamprosate - reduces cravings in abstinent alcoholics

Naltrexone - reduces rewarding effects of alcohol in abstinent alcoholics

Topiramate - reduces active drinking

Onedastron - 5ht3 antagonist, reduces cravings
Most common pathogen in neonatal CNS infection
Group B strep
Most common pathogen in pediatric CNS infection
N. meningitidis
Most common pathogen in adult CNS infection
S. pneumoniae
Most common viral pathogen in CNS infection
enteroviruses
Why do SSRIs work better in children than adults?
More sensitive seratoninergic system
Rx for aggressive autism patients
Use antipsychotics:
aripiprazole
risperidone
What is first line RX for children an adolescents with ADHD?
Stimulants:
amphetamine
Methylphenidate
What are the 3 pathways of dopamine?
Mesostriatal: SN to striatum
Mesolimbic: Ventral tegmentum to limbic system
Mesocortical: SN, VT to cortex
What are the long GABA pathways?
striatum to SN
hypothalamus to forebrain
What is the mechanism of phenothiazine (and other typical) neuroleptics?
D2 (dopamine receptor) antagonists
What are the most potent "typical neuroleptics?
Piperazine (trifluoperazine)
Butyphenones/Haloperidol
What are examples of atypical neuroleptics?
Clozapine - binds at D4; causes potentially fatal agranulocytosis

Olanzapine - safe than clozapine

Risperidone - D2 antagonist but also potent at other receptors
What are non-dopa related side effects of neuroleptics
Sedation
Orthostatic hypertension
Extrapyramidal symptoms (acute Parkinsonism, chronic tardive dyskinesia)
What are dopa-related side effects of neuroleptics?
Anti-nausea (nausea produced at chemoreceptor trigger zone by dopa)
Endocrine effects
What is the correlation of dopa with schizophrenia
anti-Dopanergic drugs relieve schizophrenia symptoms

Increase in dopa causes psychotic symptoms
What are the sidechain classes of phenolthiazines?
Aliphatic - chorpromazine
Piperidine - Thioridazine
Piperazine - Trifluoperazine