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BCN > E5 > Flashcards

E5 Flashcards

1
Q

How does Rett differ from autism?

A

Rett: universal regression

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2
Q

What is required for autism diagnosis?

A

Persistent deficits in social interaction across multiple contexts

  • -Social-emotional reciprocity
  • -Nonverbal communication
  • -Developing, maintaining, and understanding relationships

Restricted, repetitive patterns of behavior/interests/activities

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3
Q

What are the four core features of Rett syndrome?

A 
Psychomotor REGRESSION
--Language
--Hand use
Stereotypic movements (hand washing, wringing, squeezing, clapping, tapping, etc)
Gait dysfunction
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4
Q

What is the genetic mechanism of Angelman syndrome?

A

Loss of UBE3A, normally maternally inherited

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5
Q

What is the genetic inheritance of Fragile X?

A

X-linked dominant

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6
Q

What causes exophthalmos in Graves’ disease?

A

Accumulation of extracellular matrix proteins, inflammation, and fibrosis

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7
Q

What is caused by tears in bridging veins?

A

Subdural hematoma

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8
Q

What is the most common intraocular malignancy in adults?

A

Metastatic carcinoma

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9
Q

What is the most common primary intraocular malignancy in adults?

A

Uveal melanoma

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10
Q

Where does uveal melanoma typically metastasize to?

A

Liver

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11
Q

Where does uveal melanoma typically metastasize to?

A

Liver

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12
Q

Diffuse acute focal suppurative CNS infections can lead to…

A

Cerebral abscess

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13
Q

How is viral meningo-encephalitis diagnosed?

A

Increased protein
Normal glucose
Lymphocytes and macrophages in perivascular Virchow-Robbins spaces

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14
Q

Bitemporal encephalitis is ____ until proven otherwise

A

Herpes simplex

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15
Q

PML is caused by…

A

JC virus

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16
Q

PML affects what type of patient and what type of cell?

A

Immunocompromised / oligodendrocytes

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17
Q

What is the main feature of PML?

A

Demyelination

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18
Q

Histological appearance of HIV encephalitis

A

Perivascular giant cells in white matter

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19
Q

Protein conformation change in prion diseases

A

PrP-C to PrP-SC

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20
Q

What are the four ways in which guidance cues can direct connectivity?

A
  1. Graded axon guidance cues
  2. Homophilic adhesion cues
  3. Axon-axon recognition cues
  4. Sub-cellular adhesion cues
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21
Q

How are axons guided in the eye?

A
  1. Axons are directed to the optic disc (repulsed from periphery of retina, attraction to optic disc)
  2. Axons are then guided to the optic chiasm, where temporal axons are sent ipsilaterally, and nasal axons are sent contralaterally
  3. These axons reach the tectum, where a gradient exists to send axons to the proper location
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22
Q

What is a critical period?

A

Specific time in development in which activity/physiology influences responsiveness

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23
Q

In what order to critical periods open during development?

A

Vision/sensory –> language/higher function

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24
Q

T/F: Critical periods for language and higher cognition diminish, but don’t ever close

A

True

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25
Q

What is amblyopia?

A

Reduced vision in absence of overt ocular pathology

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26
Q

What is the primary cause of amblyopia?

A

Strabismus (misaligned or crossed eyes)

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27
Q

What is anisometropia and how is it treated?

A

Unequal focus due to refractive error. Use glasses to correct.

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28
Q

How does anisometropia cause amblyopia?

A

One eye is out of focus, so other one over-compensates

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29
Q

What causes the most severe form of amblyopia?

A

Cloudiness in the normal clear eye tissue or lid droop

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30
Q

How do you treat amblyopia?

A
  1. Patches
  2. Eye drops (atropine) –> temporarily blur vision in stronger eye, so patient is forced to use weaker eye
  3. Glasses –> correct refractive errors
  4. Surgery (cataracts, extraocular muscles to realign eyes in strabismus)
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31
Q

Which visual functions have relatively short periods of development?

A

Basic spectral sensitivity functions of rods and cones

3-6 months

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32
Q

Which visual functions have relatively long periods of development?

A

More complex functions such as monocular spatial vision or resolution
25 months

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33
Q

How long is the period of development for binocular vision?

A

Long, over 25 months

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34
Q

How does increasing GABA function affect critical periods?

A

Leads to premature maturation of period (early end of plasticity)

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35
Q

How does decreasing GABA function affect critical periods?

A

Leads to delayed critical period (extends period of plasticity)

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36
Q

Increased/decreased GABA leads to premature development.

A

Increased

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37
Q

What is neuroplasticity?

A

Ability of the brain to reorganize by creating new neural pathways to adapt, as it needs

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38
Q

What is the difference between explicit and implicit memory?

A

Implicit (Nondeclarative) – nonconscious – skills/behaviors
Explicit (Declarative) – conscious – facts/events

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39
Q

What type of memory does Korsakoff’s syndrome affect?

A

Explicit memory (and in some cases implicit)

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40
Q

How does chronic alcohol abuse affect memory?

A

Causes thiamine deficiency, which leads to cell death in medial thalamus and mammillary bodies

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41
Q

Damage to what structures causes complete loss of ability to form new memories?

A

Mesial Temporal System –> entorhinal and perirhinal cortices, hippo, parahippo, amygdala

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42
Q

What are two types of plasticity?

A

Functional: brain can move a function from a damaged area to an undamaged one
Structural: brain can change structure as a result of experience or learning

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43
Q

What structures of the brain are associated with implicit memory?

A

Cerebellum, basal ganglia

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44
Q

What structures of the brain are associated with Sensory memory?

A

Where (spatial) - dorsolateral prefrontal cortex

What - orbito-prefrontal cortex

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45
Q

When does consolidation of long term memory occur?

A

During sleep when serotinergic raphe nucleus neurons are active in their projection to the hippocampus

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46
Q

Where is much of the work associated with memory done in the hippocampus?

A

CA1/CA3 regions

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47
Q

Which drug blocks NMDA receptors, thereby preventing new LTP and blocking entry of Ca2+?

A

AP5

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48
Q

What are three mechanisms of synaptic plasticity?

A
  1. LTP results in insertion of new AMPA receptors into dendrites
  2. Increase in GLUT receptors = stronger potentials in active synapse
  3. Synaptic growth: dendritic spines split after LTP –> new synapses
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49
Q

Stimulation of the Schaffer collaterals generates EPSP in postsynaptic CA1 cells. What is this ideal for?

A

Facilitating memory formation

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50
Q

Which enzyme in dendrites is activated by Ca2+?

A

CaM-KII

Ca2+ binds with CaM-KII, linking proteins attached to NMDA receptor
AMPA receptors are linked to NMDA receptor by protein

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51
Q

LTP results in the insertion of new AMPA/NMDA receptors into the dendrite.

A

AMPA

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52
Q

Which receptors are ionotropic glutamate receptors, thereby creating stronger potentials in an active synapse?

A

AMPA

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53
Q

AMPA receptors are located inside the _____, but move to _______ after LTP.

A

dendrite / tips of spines

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54
Q

Additional synthesis of what molecules is required for long term memory?

A

Proteins

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55
Q

Protein synthesis inhibitors lead to deficits in ____ and _____.

A

learning / memory

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56
Q

What is GAP43? What is it involved in?

A

Protein involved in synaptic maintenance and neuritic regeneration.

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57
Q

Which protein is significantly reduced in the frontal cortex and hippocampus of Alzheimer’s patients?

A

GAP-43

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58
Q

There is a significant positive correlation between GAP-43 and the number of senile plaques in which structure?

A

Hippocampus (but not frontal cortex)

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59
Q

What is LTP?

A

Stimulation of excitatory fibers that make connections with hippocampal pyramidal cells?

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60
Q

What causes increased efficiency of CA1 pyramidal cell response?

A

Short, high-frequency stimulation of entorhinal afferents or Schaffer collaterals to hippocampal pyramidal cells over time

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61
Q

Where is alpha-synuclein predominantly expressed?

A

Hippocampus, neocortex, thalamus, substantia nigra

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62
Q

Epidermal growth factor favors differentiation into ____, whereas fibroblast growth factors promote _____.

A

glial cells / neuronal production

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63
Q

What type of gene therapy can induce neurite outgrowth from mammalian auditory neurons?

A

BDNF

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64
Q

What type of gene therapy can increase sprouting of dopaminergic axons in the striatum?

A

Glial cell line-derived neurotrophic factor (GDNF)

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65
Q

List the return to play parameters

A

In order:

  • -No activity
  • -Light aerobic exercise
  • -Sport specific exercise
  • -Non contact training drills
  • -Full contact practice
  • -Return to play
  • -Symptomatic for more than 10 days, see doctor
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66
Q

What anti-inflammatory drugs can be used after a concussion?

A

Cox inhibitors: aspirin, ibuprofen, naproxen

Cytokine blockers/microglia suppressors: minocycline, progesterone

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67
Q

Which neurotrophic drugs are used after concussion?

A

BDNF agonists: SSRI, TCA, progesterone

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68
Q

Which immune-boosting drugs are used after concussion?

A

Probiotics, vitamin D, B-glucan

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69
Q

What are the components of the SCAT3?

A
  1. GCS
  2. Maddocks score
  3. Symptoms
  4. Cognitive assessment
  5. Neck examination
  6. Balance examination
  7. Coordination examination
  8. SAC delayed examination
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70
Q

When is tau protein found in athletes?

A

In chronic traumatic encephalopathy

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71
Q

When do simple concussions resolve?

A

7-10 days

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72
Q

After concussions, children should return to ____ before return to _____.

A

learn / sport

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73
Q

When can SCAT3 be used?

A

When the patient is 13 years or older

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74
Q

Symptoms immediately following concussion

A 
Blurred/double vision
Sensitivity to light or noise
Headache
Dizziness/balance problems
N/V
Fatigue
Confusion
Trouble sleeping
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75
Q

What are post-concussion syndrome symptoms?

A 
Chronic headaches
Fatigue
Sleep problems
Personality changes
Dizziness
Short-term memory loss
Nausea
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76
Q

In most people, when do post-concussion syndrome symptoms begin?

A

Symptoms occur within first 7-10 days and go away within 3 months, though they an persist for a year or more.

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77
Q

What is the most long-term sequella of a concussion?

A

Depression

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78
Q

What is CTE?

A

Accumulation of tau protein in neurons

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79
Q

What does CTE cause?

A

Dementia pugilistica

Brain atrophy

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80
Q

Most common symptoms of CTE

A 
Aggression
Depression
Loss of memory
Loss of impulse control
Impaired judgement
Balance difficulties
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81
Q

What are the three components of concussion pathogenesis?

A

Metabolic, excitotoxic, immunologic

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82
Q

What is resveritrol?

A

Reduces brain inflammation by calming microglia and macrophages

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83
Q

When should imaging be performed if concussion suspected?

A

Neuro findings on exam, worsening symptoms, or prolonged disturbed consciousness

84
Q

What is the pharmacologic therapy for treating concussions?

A

Currently there is no evidence-based pharm. therapy available for treating concussions

85
Q

What factors can prevent concussions?

A

Hydration
Strong neck/shoulders
Genetics
Good technique

86
Q

What is the immunologic pathogenesis of concussions?

A

Elevated levels of glutamate
Decreased cerebral blood flow
Transient release of high levels of ROS, lipid peroxidation product, prostaglandins, and NO
Activation of microglia and macrophages –> increased TNF alpha, increased regulation of chemokines

87
Q

A 65-year- old woman presents today after a massive intracerebral hemorrhage. She is on the ventilator set on Assist Control at a rate of 14. She is breathing 16 times per minute according to the nurse’s flow sheet; the respiratory therapist trouble shoots the ventilator to make sure that the excess breaths are not an artifact.Her physical examination shows no evidence of brain stem function (all the tests are consistent with death). Your next step would be:

A. Declare the patient dead

B. Proceed to apnea testing

C. Counsel the family that she is not going to die

D. Retest the patient in a few hours

A

D

88
Q

A 43-year- old man with a history of insulin dependent diabetes presents after a traumatic brain injury. He is 36 C° and has the following laboratory values:

 Na 135 mmol/L

 K 4.2 mmol/L

 Glucose 475 mg/dL

His physical exam shows no brain stem function, he is not breathing over the ventilator. His apnea test shows no effort despite an increase of pCO2 of >20 mmHg (42 mmHg to 65 mmHg).

The next appropriate step would be to:

A. Declare the patient dead

B. Repeat the apnea test

C. Control his blood glucose prior to retesting him

D. Counsel the family that he is likely not going to die

A

C

89
Q

A 24-year- old man presents to the ICU in a coma. There are no outward signs of trauma, his head CT done 24 hours after admission is normal without evidence of stroke or hemorrhage. On examination and apnea testing, he meets all the criteria for death. The next appropriate step would be to:

A. Consider drug intoxication

B. Declare the patient dead

C. Increase his body temperature to 38 C°

D. Repeat the apnea test

A

A

90
Q

An 18-year-old patient comes to the ICU after a near-drowning episode in the winter. The patient has a core body temperature of 27 C°.The physical examination and apnea test are consistent with brain death. The next appropriate step is to:

A. Declare the patient dead

B. Warm the patient and repeat testing

C. Test for drugs of abuse

D. Do an ancillary test to confirm death

A

B

91
Q

A 32-year- old man presents to a trauma ICU after a suicide attempt with a gun where he caused significant damage to the right side of his face and right eye. The exam components that are assessable are consistent with death and his apnea test is also consistent. The next appropriate step is to:

A. Declare the patient dead

B. Talk to the family about whether his face worked normally before the gunshot wound

C. Assess for drugs of abuse

D. Proceed to ancillary testing to confirm the diagnosis

A

D

92
Q

Which of the following examination findings is consistent with death?

A. Fixed right pupil with sluggishly reactive left pupil

B. Extensor posturing in the legs and arms with painful stimulation

C. Eye deviation without nystagmus on oculovestibular (cold-caloric) testing

D. Eyes that remain the midline with lateral head movement

A

D

93
Q

Which of the following blood laboratory findings could be considered a confounding factor in the diagnosis of death?

A. Magnesium level of 2.1 mg/dL

B. WBC count of 12 k/L

C. Sodium of 118 mmol/dL

D. Potassium of 4.0 mmol/dL

A

C

94
Q

Which medication is most likely to confound the diagnosis of death by neurological criteria?

A. Sodium pentobarbital

B. Ranitidine

C. Acetaminophen

D. Metoprolol

A

A

95
Q

Which of the following conditions invalidate all ancillary tests?

A. Facial injuries making complete cranial nerve testing impossible

B. Hypotension on apnea testing causing abortion of the test

C. Patients with left ventricular assist devices

D. Severe Hypothermia

A

D

96
Q

Which ancillary test is not validated yet in patients for the diagnosis of death by neurological criteria?

A. CT angiography

B. Digital Subtraction Angiography (convention angiogram)

C. EEG

D. Radionuclide Scintigraphy (nuclear testing)

A

A

97
Q

What does MS treatment involve?

A

Disease modification as well as symptomatic treatment of fatigue, depression, and pain

98
Q

What is used to treat acute MS exacerbations?

A

Corticosteroids

99
Q

In MS, loss of myelin leads to increased intracellular ____ and _____.

A

calcium / sodium

100
Q

Which disease-modifying MS drugs are generally safe and well-tolerated, and require self-injection?

A

IFN-B
Natalizumab
Glatiramer acetate

101
Q

Which disease-modifying MS drugs are administered orally?

A

Fingolimod
Teriflunomide
Dimethyl fumarate

*These drugs are not as safe

102
Q

What corticosteroid is administered for MS exacerbations?

A

IV methylprednisolone 500 mg/day for five days, followed by optional oral prednisone

103
Q

What is the mechanism of action of IFN-B in modifying MS?

A

Interferes with target recognition.
Switches TH1 inflammatory response to TH2 anti inflammatory.
Reducing T-cell activation and BBB crossing
Decreasing metalloproteases (MMPs)

104
Q

Glatiramer acetate

A

The Decoy Gladiator:

Wears reversible armor that looks like myelin on the outside so when the relapsers come, he will
be attacked, but the real myelin stays safe. (REDUCES FREQUENCY OF RELAPSE)

The suit is automatic. He just flips a switch and it reverses from type 1 to type 2 (SHIFTS TH1 –> TH2)

The armor is tight around his chest, though, and creates some pain and the TH1/TH2 button is on the inside and leaves a mark on his arm. (CHEST TIGHTNESS AND INJECTION SITE REACTION)

105
Q

Fingolimod

A

Fingers Schmingers

Modulates Sphingosine-1-phosphate (S1P1) receptor.

Fingers Schmingers can do things regular fingers can’t like grab the lymphocytes and stick them back where they belong - Like in the lymphoid organs.

Hold up two fingers. Those are the two months this shit stays in yo system. Now check your pulse with them. It’s bradycardia! Let’s do more with our fingers. Can you check your BP with them? I bet it’s high. Fingers Schmingers are actually not under your control any more. They poke your liver with them. Bet that hurt. Now for the final fingers schmingers trick, those fingers jam themselves deep in your macula until it causes edema. The only way to stop them is to give them cancer.

Bradycardia, high BP, macular edema, melanoma

106
Q

Fingolimod MOA

A

Makes S1P receptors non-functional –> prevents T-cell invasion of CNS

107
Q

Dimethyl fumarate

A

Fumar Mentoles. Translated - smoke menthols.

They feel good in my mouth (oral). I smoked regular cigarettes but the smell stayed with me like glue. The menthol somehow inhibits the expression of all those adhesion molecules (inhibits adhesion molecule expression) and I don’t taste the chemicals at all (chemokine inhibition). The smell doesn’t grab me like a macrophage (suppresses macrophages). It protects me like, well, a Nerf helmet (increases Nrf2 DNA binding). I even got a little tattoo on the back of my neck at C6 of a star smoking a menthol (suppresses astrocytes and C6 glioma cells). They even give me health benefits, like a nice healthy flush to my face (flushing) and they help me poop (diarrhea).

108
Q

Which MS drugs should not be given to pregnant women?

A

Teriflunomide, Mitoxantrone

109
Q

Which MS drug can cause PML?

A

Natalizumab

110
Q

Natalizumab MOA

A

Monoclonal antibody against alpha-4-integrin

111
Q

Natalizumab should not be given to which patients?

A

Immunocompromised

112
Q

Mitoxantrone

A

Mitoxantrone is so toxic, nothing can grow around it, no new growth and no abnormal growth. It is double toxic and suppresses B and T immunity. Works for all MS but primary because primary progressive never remits and gives the toxicity a chance. And, it is also the most toxic to the body. Neutropenia, Thrombocytopenia, AML, CHF, Liver, GA, and you sure don’t want to give that to a fetus.

113
Q

Ocrelizumab

A

You like okra? I do. I am an expert, see: Funny fact - did you know if you cut okra open, there are exactly 20 seeds (CD20) visible? Pretty cool. (ocrelizumab is a monoclonal antibody for CD20).

You know who taught me about 20 Seeds? My Jamaican GramMa, Tuxxy. She sure had a fatty bum from eatin so much okra! (riTUXimab and oFATUMumab also target CD20)

I crave that shit. My cravings come and go but keep getting worse the longer I don’t eat any. It’s like my cravings are progressive and relapsing.

Ocrelizumab is only FDA approved for Progressive-relapsing MS. So when you see Progressive-Relapsing MS, remember my progressive-relapsing craving for okra

114
Q

Dalfampridine

A

Hey, I invented a new word. Hey Poboy, why don’t you dalfamper your ass over here. It’s like dollying and scampering; like how he walks. And when he walks, he says OK OK OK OK. (K+ channel block) Dalfampridine helps speed up gait but when you see the $15,000 a year price, you will certainly have a seizure.

115
Q

What does brain death diagnosis require?

A

Demonstration of the absence of both cortical and brainstem activity

116
Q

What is the medical criteria for diagnosing brain death?

A

Absence of cerebral function
Absence of brainstem function
Apnea test

117
Q

What is Lazarus Sign?

A

Spinal cord reflexes that persist even with diagnosis of brain death

118
Q

What is the Apnea Test?

A

Test for absence of respiratory function:

  1. Preoxygenate 100% –> take baseline ABG –> disconnect ventilator –> administer O2 –> observe respirations –> draw ABG in 8-10 minutes
  2. pCO2 > 60 mmHg or 20 mm Hg above base
119
Q

When should you abort an apnea test?

A
  1. Patient breathes
  2. Hemodynamic instability
  3. Inconclusive if no respiratory movement but pCO2 < 60 mmHg
120
Q

Brain death: cerebral angiogram findings

A

No intracerebral filling at level of carotid bifurcation or circle of Willis

121
Q

Brain death: cerebral blood flow–nuclear scan findings

A

No uptake of radionuclide in brain parenchyma

“Hollow skull phenomenon”

122
Q

Brain death: TCD findings

A

No diastolic flow, systole only retrograde diastolic flow

123
Q

Brain death: EEG findings

A

No electrical activity for 30 minutes

124
Q

Drugs used for episodic migraine prevention

A

Beta blockers: propanolol, timolol

Also: topiramate, divalproex sodium

125
Q

Drugs used for chronic migraine prevention

A

Botulinum toxin A

126
Q

Botulinum MOA

A

Blocks release of substance P and CGRP

127
Q

Drugs used for acute migraine treatment

A

Triptans
Dihydroergotamine
Diclofenac

128
Q

Triptans MOA

A

Agonist of 5-HT1-B/D presynaptic receptor / inhibits terminal excitability / vasoconstrictor

129
Q

Which drugs should not be used within two weeks of taking MAOIs?

A

Triptans

130
Q

What are the pros of using beta blockers for migraines?

A

Widely used

FDA approved: Timolol, Metoprolol, Propanolol

131
Q

What are the cons of using beta blockers for migraines?

A

Side effects: fatigue, dizziness, depression, may worsen aura

132
Q

Which patients should not take beta blockers?

A

Those with ASTHMA, depression, bradycardia, Raynaud’s, CHF

133
Q

Common side effects of divalproex sodium

A

Tremor, bruising, nystagmus

134
Q

Rare side effects of divalproex sodium

A

Pancreatitis, alopecia, thrombocytopenia

135
Q

Drugs used for menstrual migraines

A
  1. Frovatriptan
  2. Naratriptan, Zolmitriptan
  3. Estrogen
136
Q

Which menstrual migraine medication is the most long-acting?

A

Frovatriptan

137
Q

Drugs used to treat acute migraine

A

Sumatriptan
DHE
Diclofenac

138
Q

Diclofenac MOA

A

COX inhibitor –> reduces PROSTAGLANDINS –> reduced inflammation

139
Q

Acute headache treatment should be limited to what time frame?

A

2-3 days per week

140
Q

Drugs used to treat acute cluster headaches

A

Oxygen
Sumatriptan
Indomethacin

141
Q

Drugs used to treat chronic cluster headaches

A

Verapamil
Lithium
Deep brain stimulation

142
Q

Drugs used to treat headaches associated with neuralgia

A

Carbamazepine

Gabapentin

143
Q

Nerves associated with headaches in the front and back of head

A

Front: branches of trigeminal
Back: branches of first three cervical nerves

144
Q

Overuse definition: ergotamines/triptans/opioids

A

More than 10 days per month for 3+ months

145
Q

Overuse definition: simple analgesics

A

More than 15 days per month for 3+ months

146
Q

Which migraine drug is offered as a generic?

A

Rizatriptan

147
Q

What is the only triptan considered superior to sumatriptan?

A

Eletriptan

148
Q

Which migraine drugs are teratogenic?

A

DHE, topiramate

149
Q

Which NT is depleted during a migraine?

A

Serotonin

150
Q

Opioid overdose deaths are most common in which age group?

A

45-54

151
Q

Neurotoxic side effects of opioids

A

Myoclonus, hyperalgesia, delirium, hallucinations

152
Q

______ should not be given to elderly patients.

A

Meperidine

153
Q

What is an indication of hyperalgesia due to opioid use?

A

Myoclonus during sleep

154
Q

M6G is more/less potent than M3G

A

More

155
Q

Which factors can increase accumulation of morphine metabolites?

A

Age > 70 years, renal failure, dehydration

156
Q

Naloxone does/does not reverse neuroexcitatory effects

A

Does not

157
Q

What is the only intervention with efficacy for the treatment of chemotherapy-induced peripheral neuropathy?

A

Duloxetine

158
Q

Duloxetine MOA

A

SNRI

159
Q

All drugs of abuse increase which NT?

A

Dopamine

160
Q

What is the mesolimbic dopamine system?

A

Key component of the brain reward system

161
Q

MDS neurons originate in _____ and project to neurons in ______

A

VTA / nucleus accumbens

162
Q

THC partially binds to ____ receptor

A

CB1

163
Q

Clinical manifestations of stroke

A 
Abrupt onset hemiparesis, monoparesis
Hemisensory deficits
Monocular/binocular visual loss
Diplopia
Dysarthria
Facial droop
Ataxia
Vertigo
164
Q

Best imaging method to diagnose CVA

A

Non-contrast CT

165
Q

Describe the anatomy of the cavernous sinus

A

CNs III, IV, V1, V2, VI
ICA
Orbital vein into, out to petrosal sinuses

166
Q

What is delirium?

A

Fluctuating LOC +/- cognitive impairment

167
Q

What are the five most common causes of first time seizures in a patient 15 years or older?

A 
Idiopathic
Cerebral infarction
Alcohol withdrawal
CNS infection
Tumor
168
Q

Von Hippel-Lindau

A

Hemangioblastoma

169
Q

Tuberous sclerosis

A

Subependymal giant cell astrocytoma

170
Q

NF type I

A

Optic glioma
Astrocytoma
Neurofibroma

171
Q

NF type II

A

Acoustic neuroma
Meningioma
Ependymoma
Astrocytoma

172
Q

Li-Frumeni

A

Astrocytoma

PNET

173
Q

Turcot syndrome

A

Glioblastoma

Medulloblastoma

174
Q

What is the Monroe-Kellie Principle?

A

The cranium is a closed container, so increase in volume in one element must be balanced by decrease in another element.

175
Q

Clinical signs of brain herniation

A 
Brainstem compression (mydriasis, posturing, LOC)
Eye findings (e.g. loss of conjugate movement)
Cushing reflex
176
Q

What type of strokes are inoperable?

A

Basal ganglia

177
Q

Where are most brain aneurysms located?

A

Anterior circulation (90-95%)

178
Q

Brain aneurysm risk factors

A 
Family history
Age > 50 years
Female
Current smoker
Cocaine use
Binge drinking
179
Q

CN III palsy + ptosis
Dilated unreactive pupil
Ophthalmoplegia

A

Posterior communicating aneurysm

180
Q

Most common cause of spinal epidural abscess

A

Hematogenous spread

181
Q

Red flag symptoms of back pain

A

Trauma
Unexplained weight loss
Neuro symptoms
Age > 50

Fever
IVDU
Steroid use
History of cancer

182
Q

MRSA + epidural steroid injections = ______

A

Spinal abscess

183
Q

What type of injury is most likely to produce a contrecoup injury in the inferior frontal lobes, temporal tips, and inferior temporal lobes?

A

A fall backward

184
Q

Basal ganglia putaminal hemorrhage is most likely to occur in _______.

A

hypertension

185
Q

Red shrunken neurons are typically seen in response to _____.

A

Global hypoxia

186
Q

Histologic finding of rabies

A

Negri bodies

187
Q

Immunocompromised
Produces abscesses that organize on the periphery
Bright ring on CT and MRI

A

Toxoplasma

188
Q

Pilocytic astrocytomas with _____ mutations tend to be less circumscribed.

A

BRAF

189
Q

Negative for GFAP, positive for CD19 and CD20

A

Diffuse large B-cell lymphomas

190
Q

GBMs often have ____ alterations.

A

EGFR

191
Q

Bilateral acoustic schwannomas

A

NF 2

192
Q

The scarring following bacterial meningitis can lead to _____________, or alternatively scarring at the arachnoid granulations to reduce CSF reabsorption and produce communicating hydrocephalus.

A

obstruction of CSF flow at the foramina of Luschka and Magendie with obstructive non-communicating hydrocephalus

193
Q

Methanol is metabolized to what toxic compounds?

A

Formic acid and formaldehyde

194
Q

_________ loves to invade blood vessels and produce thrombosis. _________ is a risk for aspergillosis.

A

Aspergillus / Neutropenia

195
Q

A premature child is at risk for germinal matrix hemorrhage, which often extends into the _______ region

A

intraventricular

196
Q

Edema is most likely to be severest in which part of the brain?

A

White matter

197
Q

MS: Histology

A

Perivascular lymphocytes with demyelinated axons in white matter

198
Q

Foci of multinucleated cells and macrophages in grey and white matter

A

HIV encephalopathy

199
Q

Affected brains are typically atrophic, with enlarged ventricles, and show accumulation of tau-containing neurofibrillary tangles in superficial frontal and temporal lobe cortex, which can be similar to Alzheimer disease.

A

CTE

200
Q

Berry aneurysms are associated with what condition?

A

Autosomal dominant polycystic kidney disease

201
Q

Granulation tissue with fibrosis is a typical healing inflammatory response reaction to ______.

A

a cerebral abscess

202
Q

Vincristine MOA

A

Microtubule inhibition: tubulin molecules fail to polymerize

203
Q

Paclitaxel MOA

A

Microtubule inhibition: unusually stable tubulin molecules fail to depolymerize

204
Q

A 14-year-old boy is brought to the emergency room following an accident in which he hit his head against a concrete wall. He was initially unconscious but then regained alertness 5 minutes later. However, an hour later in the emergency room, he is comatose, and skull radiograph reveals a linear skull fracture of the temporal-parietal region on the left. What is most likely develop in this boy?

A

Epidural hematoma

The ‘lucid’ interval is classic for an epidural hematoma from a tear of the middle meningeal artery. The hematoma accumulates rapidly, because the bleeding is arterial.

205
Q

A 45-year-old man has had a severe, intractable headache for a week. Physical examination reveals papilledema on the right. A head CT scan shows marked right to left midline shift. MR imaging shows a 6 cm enhancing mass lesion in the right parietal region with marked surrounding edema. He then develops a dilated pupil on the right. What is the most likely vascular lesion?

A

Pontine hemorrhage

206
Q

Too rapid correction of hyponatremia can lead to _____.

A

CPM: central pontine myelinolysis

BCN (6 decks)

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