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32 Cards in this Set

  • Front
  • Back
If a patient's Vitamin B12 level is borderline low, what should you consider?
Check homocysteine/methylmalonic acid.
True/False: Vitamin B12 deficiency can be treated with po vitamin B12.
True.
HIV- associated dementia: where does it affect the brain first?
Basal ganglia and substantia nigra.
HIV- associated dementia: Why does it matter what part of the brain gets affected?
May explains why haldol/risperidal are not best first choices for rx – high rate of dystonia.
HIV- associated dementia: What are risk factors?
High viral load.
HIV- associated dementia: When to screen for this?
CD4<350.
HIV- associated dementia: Diagnostic differential?
Opportunistic CNS infections, delirium, depression.
HIV- associated dementia: What are other risk factors?
Low education, older age, IV drug use, anemia, female.

stinky mnemonic: Le Oaaf IV
HIV- associated dementia: What are the symptoms?
subcortical dementia (think APRIL AGE) – apathy, depression are prominent, Parkinsonism psychosis, mania

stinky mnemonic: SD MAD PP
HIV- associated dementia: What is the course of the disease?
Varies, can be slow, but on average: Rapid progression – death in 2 years.
HIV- associated dementia: How do you diagnose it?
MRI to r/o other causes.
HIV- associated dementia: How do you treat it?
antiretrovirals.
Name 3 ways Hepatitis C or its treatment can affect behavior. Explain how the conditions affect brain function.
1) Acute fulminant hepatitis (rare) / Cirrhosis (common)
- can damage liver function enough to increase NH3.
2) Inflammatory cytokines
- adversely affect brain function.
3) Interferon can precipitate depression
- Interferon is a pro-inflammatory cytokine.
Name 3 conditions commonly comorbid with hepatitis C that affect behavior.
1) HIV can be comorbid – Hep C does not affect brain directly, but HIV does.
2) EtoH use/drug use is common comorbidity
3) Alzheimer’s Disease

stinky mnemonic: HEDAD
Alzheimer’s Disease: Pathophysiology of Cortical Dementia: where does cortical atrophy occur?
ACh neurons in nucleus basalis; also association cortex of temperoparietal lobe and (to lesser degree) frontal lobes.
most severe: medial temporal, includes hippocampus.
Alzheimer’s Disease: Yes/No: Are subcortical structures involved even though this is a “cortical dementia”?
Yes.
Alzheimer’s Disease: What are the classic microscopic findings?
Senile plaques, neurofibrillary tangles, neuronal and synaptic loss, granulovascular degeneration of neurons, amyloid angiopathy.
Alzheimer’s Disease: Which of the microscopic findings are unique to Alzheimer disease?
Amyloid plaques.
Alzheimer’s Disease: What are neurofibrillary tangles?
Mostly phosphorylated tau protein: these are seen in other neurodegenerative diseases
Alzheimer’s Disease: What are tau proteins?
part of cytoskeleton
Alzheimer’s Disease: What are the DSM IV-TR criteria for Dementia of the Alzheimer’s Type:
Criterion A: multiple cognitive deficits:
Loss of memory +
At least one of: Agnosia, Apraxia, Aphasia
Criterion B: Impaired executive function
Criterion C: Gradual onset, continuing cognitive decline
Subtypes:
Early Onset: <age 65
Late Onset: > age 65
Alzheimer’s Disease: Name two classes of meds, give one example each and the mechanism of action.
Cholinesterase inhibitors (Donezepil)
decreased Ach from involvement of nucleus basalis of Meynert
Glutamate antagonist (Memantine)
protects neurons from glutamate which can be neurotoxic
Alzheimer’s Disease: Name characteristics of subcortical dementia that are different from in cortical dementia and how they are different.
stinky mnemonic: APRiL AGE
A pathy
P sychomotor Retardation
R ecall (unlike cortical dementia, recall better preserved, can be better with cues)
iL = L oss of Initiative
A ffective Syndrome
G ait
E xtrapyramidal Signs
All are earlier or more marked (except for recall)
What kind of dementia(s) is/are probably responsive to anti-cholinesterase inhibitors?
Alzheimer’s, Lewy Body/Parkinsons, Vascular, maybe dementia from TBI.

stinky mnemonic: VALP TBI
What kind of dementia(s) is/are less likely to be responsive to anti-cholinesterase inhibitors?
Huntington, Frontotemporal.
Secondary Parkinson’s symptoms: Name 6.
Bradykinesia, Extrapyramidal Rigidity, Rest Tremor; Festinating gait, Masked facies

stinky mnemonic: BERT FM
Striatum:
Name a major component of the ventral striatum.
Nucleus accumbens.
Striatum:
Name two components of the dorsal striatum.
Caudate and Putamen.
In the striatum, the direct pathway is mediated by the ___ receptor, while the indirect pathway is mediated by agonism of the ___________receptor or antagonism of the ________receptor.
the direct pathway is mediated by the __D1__ receptor.
the indirect pathway is mediated by agonism of the __serotonin/5HT__ receptor or antagonism of the __D2__ receptor.
The direct pathway ________ action while the indirect pathway __________________ This may explain (list two clinical observations):
The direct pathway __facilitates (Go)__ action while the indirect pathway __inhibits action (NoGo)__ This may explain:
1) Serotonin decreases impulsivity.
2) Dopamine increases impulsivity.
Deep brain stimulation for Parkinsons disease inhibits ________ activity, thereby reducing the __________ pathway activity and the __________ Signal.
Deep brain stimulation for Parkinsons disease inhibits __STN__ activity, thereby reducing the __hyperdirect and indirect__ pathway activity and the __Global NoGo__ Signal.
Deep Brain Stimulation of this structure is associated with decreased ability to ___________when it is unclear what the reward/risk ratio is.
Deep Brain Stimulation of this structure is associated with decreased ability to __wait for more information__ when it is unclear what the reward/risk ratio is.