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Quiz 4 Flashcards

1
Q

Identify the following:
Pituitary stalk
Mammillary bodies
Tuber cinereum

A
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2
Q

What are the three neural afferent pathways of the Hypothalamus? What function is performed by each pathway?

A
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3
Q

What are the four circulatory afferent pathways of the Hypothalamus? What is the function of each pathway?

A
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4
Q

What do neurons in the periventricular nucleus of the hypothalamus produce? Where in the hypothalamus is it found? What other nuclei have similar functions?

A

Arcuate neurons have the same function
Paraventricular neurons produce CRH

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5
Q

What hormones are produced by the supraoptic nucleus of the hypothalamus?

A

ADH
Oxytocin

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6
Q

Which nuclei and molecules are involved in stimulation of sleep by the hypothalamus? Which are involved in wakefulness?

A
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7
Q

Where are the 5 most important thalamic nuclei to know for step 1?

A
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8
Q

What are the functions of the following hypothalamic neurons?
Dopamine neurons
Vasopressin neurons
Histamine neurons
GABA/galanin neurons
Hypocretin (orexin) neurons

A
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9
Q

What are the steps involved in the circuit of papez (limbic system) What two additional structures help to modify functionality of this system?

A

Note that it is an anatomic circuit, not so much a functional one

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10
Q

What area of the limbic system anatomy is disrupted in Wernicke/Korsakoff syndromes?

A
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11
Q

What are the labeled areas of the brain in this picture? (emphasis on limbic system)

A
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12
Q

What are the two most common causes of limbic amnesia? Which structure in the limbic system is affected?

A
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13
Q

What are the two most common causes of bilateral medial temporal lobe damage? What limbic structure is most often damaged? What type of amnesia is associated?

A

Note that a Bilateral PCA stroke could cause damage to this area

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14
Q

What are the three major anatomical divisions of the amygdala? What are the two major efferent pathways?

A
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15
Q

Which efferent pathway of the amygdala connects it to the frontal cortex, basal ganglia, and motor functions of the brain? What does the other pathway connect it to?

A
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16
Q

Where do the medial olfactory tracts relay sensory information to in the brain? What main area does it traverse? Where do the lateral olfactory tracts relay information to and which areas does it traverese?

A
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17
Q

Define the following:
Anosmia
Hyposmia
Parosmia
Agnosia
Dysosmia
Phantosmia
Cachosmia

A
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18
Q

What is Kallman Syndrome? What two major signs are characteristic? What is the embryological etiology?

A
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19
Q

Provide definitions for the following types of primary myelin diseases:
Demyelinating
Dysmyelinating
Hypomyelinating
Myelinolytic

A

Demyelinating- Inflammatory, sporadic immune-mediated destruction of normal myelin in the CNS

Dysmyelinating (leukodytrophies)- Non-inflammatory destruction of chemically abnormal myelin that may involve CNS or PNS (note they are heritable)

Hypomyelinating- General scarcity of normal myelin deposition during development

Myelinolytic- Non-inflammatory and sporadic. Usually intramyelinic edema in biochemically normal myelin

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20
Q

What damage to the brain is associated with Decerebrate posturing versus Decorticate posturing?

A

Decerebrate posturing- tends to occur with compromised midbrain function
Decorticate posturing- tends to occur with lesions involving the thalamus or large hemispheric masses that compress the thalamus from above

Note that decerebrate posturing generally has a worse prognosis

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21
Q

Why can tonsillar herniation produce difficulty breathing?

A

Herniation of the cerebellar tonisls through the foramen magnum cancompress the medulla (specifically the respiratory and cardiovascular centers)

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22
Q

What are personality disorders? Why are they not diagnosed until adulthood?

A

Personality disorders are patterns of pervasive, inflexible traits that lead to maladaptive behaviors and impairment

Traits are not disorders

Teens cannot be diagnosed until adulthood before of the long duration for criteria (and amount of variabliity and change)

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23
Q

What characterizes Schizoid Personality Disorder?

A
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24
Q

What characterizes Schizotypal Personality Disorder?

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25
Q

What characterizes Paranoid Personality Disoder?

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26
Q

What characterizes Histrionic Personality Disorder?

A
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27
Q

What characterizes Borderline Personality Disorder?

A
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28
Q

What characterizes Antisocial Personality Disorder?

A
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29
Q

What characterizes Narcissistic Personality Disorder?

A
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30
Q

What characterizes Avoidant Personality Disorder?

A

Differs from schizoid PD in that patients WANT social interaction but don’t feel confidant in participating unless they are SURE they will be liked

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31
Q

What characterizes Dependent Personality Disorder?

A
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32
Q

What characterizes Obsessive Compulsive Personality Disorder?

A

OCPD tends to be egosyntonic, or in harmony with the patient’s goals and needs (whether it actually is comprises a separate issue, it is PERCEIVED that way), while OCD tends to be egodystonic, or in the way of the patients desired goals

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33
Q

Define the following terms:
Countertransference
Transference

A

Countertransference- The physician’s feelings and attitudes towards the patient

Transference- The patient’s feelings and attitudes towards the physician

Both of these can be influenced by prior experiences with the other person, and even personal experiences earlier in life

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34
Q

What are the 8 steps on the spectrum of consciousness? Which two steps are normal modes of consciousness?

A

Brain death is the complete absence of consciousness

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35
Q

What are the differences between the following stages of consciousness?
Sleepy
Lethargy
Delirium
Obtunded

A
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36
Q

Which personality disorder may benefit the most from dialectal behavioral therapy (DBL)?

A

Borderline personality disorder

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37
Q

What are the criteria for diagnosing Neurofibromatosis type 1 (NF1)?

A

One must meet two of the following criteria:
- 6 or more cafe au lait spots that are >5mm diameter (pre-pubertal) or >15mm in diameter (post-pubertal)*
- 2 or more neurofibromas*
-Axillary/inguinal freckling
-Optic glioma
- 2 or more Lisch nodules*
-Bony abnormalities
-First degree relative with NF1*

  • Most classic features
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38
Q

What is the heritability and penetrance of NF1?

A

Autosomal dominant

Full penetrance with high variable expression

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39
Q

How do NF1 and NF2 differ in the following aspects?
Gene mutated
Presence/size of cafe au lait spots
Lisch nodules
Neurofibromas
Cognitive impairment
Rarity
Cancer association

A

NF1
- neurofibromin mutation
-larger cafe au lait spots
-Lisch nodules and neurofibromas
-cognitive impairments can be associated
-more common

NF2
-merlin mutation
-If present, cafe au lait spots are smaller
-No Lisch nodules or neurofibromas
-Not associated with cognitive impairment
-More cancer association (especially schwannomas, meningiomas, ependymomas)

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40
Q

Based on these skin and ocular findings, what neurocutaneous syndrome is most likely?What is the heritability? What are other notable findings?

A
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41
Q

Based on these skin and ocular findings, what neurocutaneous syndrome is most likely?What is the heritability? What are other notable findings?

A
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42
Q

Based on these skin and ocular findings, what neurocutaneous syndrome is most likely?What is the heritability? What are other notable findings?

A
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43
Q

Based on these skin and ocular findings, what neurocutaneous syndrome is most likely?What is the heritability? What are other notable findings?

A
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44
Q

Based on these skin and ocular findings, what neurocutaneous syndrome is most likely?What is the heritability? What are other notable findings?

A
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45
Q

Based on these skin and ocular findings, what neurocutaneous syndrome is most likely?What is the heritability? What are other notable findings?

A
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46
Q

What is the definition of a stroke?

A

Ischemic strokes are must more common in western culture, representing roughly 85% of strokes

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47
Q

What is the definition of a TIA?

A
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48
Q

What characterizes a thrombotic stroke? Are smaller or larger vessels affected? What two conditions can predispose patients to a higher risk for this type of stroke?

A
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49
Q

What characterizes an embolic stroke? What differentiates it from a thrombotic stroke? What are three cardiac contributors to risk for embolic stroke?

A
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50
Q

What characterizes a watershed stroke?

A

Hypo-perfusion of the most distal branches of end arterioles of major vessels
-Where ACA meets MCA
-Where MCA meets PCA

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51
Q

How can a watershed stroke be prevented/treated?

A

1) Prevent hypotension
2) Maintain euvolemia
3) Maximize cardiac output

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52
Q

What characterizes a lacunar stroke? What is another name for it?

A
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53
Q

What are three notable signs of an ACA stroke?

A
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54
Q

What are notable signs of an MCA stroke?

A
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55
Q

What are notable signs of a PCA stroke?

A

Thalamic pain syndrome is only present some of the time

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56
Q

How can a posterior circulation stroke be easily differentiated from an anterior circulation stroke?

A
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57
Q

What is the difference between the actual stroke as well as the penumbra?

A
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58
Q

A patient with signs of fever, leukocytosis and stroke is pathognomonic for what until proven otherwise?

A

Splinter hemorrhages are a classic sign

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59
Q

What are examples of inflammatory and non-inflammatory arteriopathies?

A
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60
Q

What is amaurosis fugax?

A

Note it is a type of TIA

It is a harbringer of stroke and should always be considered a medical emergency

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61
Q

When a patient presents with symptoms of stroke, what is the imaging of choice used to differentiate if it is ischemic or hemorrhagic?

A
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62
Q

Describe the findings seen on CT without contrast of both an ischemic and hemorrhagic stroke?

A

Absence of signs of hemorrhage can be an indicator of ischemia

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63
Q

What are the 3 main things (not an exhuastive list) that CT scans are used to detect?

A

Blood
Bullets
Bone

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64
Q

What is the timeframe to administer t-PA? What is the major risk it carries? What are 3 notable (not exhaustive) situations where it is contraindicated?

A

Note that in some individuals the window for t-PA administration can be extended to 4.5 hours

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65
Q

What are two advantages of interarteral or IA t-PA administration?

A
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66
Q

What is the cutoff for significant benefit with a carotid endarteretomy? What are the four main indications for the procedure?

A
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67
Q

What is the most important modifiable risk factor for stroke in a patient?

A
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68
Q

What are 4 notable signs that point to an intracranial hemorrhage?

A

Note that 70% of IC hemorrhage are due to hypertension

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69
Q

What imaging is first line in the evaluation of intracranial hemorrhage (i.e. subarachnoid hemorrhage)? What should be done if no evidence is found but suspicion persists? What can be diagnosed by CT angiography?

A
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70
Q

What is the difference between multiple sclerosis and acute disseminated encephalomyelitis?

A

MS: Demyelinating disease that occurs with chronically relapsing/remitting symptoms
ADE: Demyelinating disease that occurs only at one instance in time

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71
Q

What is the classic definition of multiple sclerosis?

A

2 clinical atatcks
2 separate locations in CNS (i.e. 2 different symptoms)
Separated by 6 months (to imply ongoing inflammation)

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72
Q

What are the signifiance of “black holes” or “enhancing lesions” seen on an MRI of a patient with multiple sclerosis?

A
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73
Q

In what two diseases is cyto-albuminemic dissociation seen? Are there exceptions?

A

GBS
MS

In MS with active demyelination, leukocytes will be ELEVATED

74
Q

What is the indicated treatment for acute inflammation in the CNS? (i.e. MS or acute disseminated encephalomyelitis)

A
75
Q

What is a common side effect of interferon therapy (as often used for chronic CNS inflammation)?

A

Serious depression

76
Q

Would imaging with areas of enhancing lesions of the same degree of enhancement be more indicative of MS or acute disseminated encephalomyelitis?

A

Acute disseminated encephalomyelitis, as it is monophasic and the lesiosn should be the same “age”.

In MS there are stages of activation and remission, and multiple lesions at varying degrees of activation may be seen.

77
Q

What is the presentation for Progressive multifocal leukoencephalopathy? How quickly does it progress? What infctious agent is responsible for causing PML? What are the two most important elements of treatment?

A

Note that inflammation is NOT a major characteristic of PML. Therefore leukocytosis is NOT characteristic of PML.

78
Q

What is the presentation of Central pontine myelinolysis? What conditions predispose a patient to it? What impacts the risk of CPM? How good are outcomes for treatment? How quickly should serum sodium levels be raised in hyponatremia?

A

Serum sodium levels should be raised NO MORE THAN 12 points in 24 hours

79
Q

How does the presentation of adrenoleukodystrophy differ in infancy, childhood and adulthood? What does the biochemical defect result in? How is it inherited?

A
80
Q

What is the difference between the following?
Minimally conscious state
Vegetative state
Coma
Brain death

A

A minimally conscious state differs from an obtunded state in that there is not CONSISTANT appropriate interaction with the environment

81
Q

What are the six major herniation syndromes to know for step 1? Which number represents which syndrome?

A

Note that a central herniation is a bilateral uncal herniation

82
Q

What is the difference between an uncal hernation and a central herniation?

A
83
Q

How is delirium described in context of states of consciousness?

A

It is a cycling between abnormal states of consciousness

84
Q

Most patients with severe brain injury or who are in the neurocritical care unit are in what conscious state?

A

Minimally conscious state

85
Q

What are two major differences between a vegetative state and a coma?

A

Patients in a coma cannot survive without life support.

As a medical student, do not chart a vegetative state. Check with your attending.

86
Q

What characterizes Locked-In Syndrome? What part of the brainstem is infarcted to produce this syndrome?

A
87
Q

What are the 3 behaviors measured in the Glasgow Coma scale? What are the significant three score values?

A
88
Q

What is cerebral palsy? How quickly does it progress? How does it rank in causes of childhood disaiblity?

A
89
Q

What are the two major types of cerebral palsy? What characterizes each? What are the three subtypes of spastic cerebral palsy?

A
90
Q

What is kernicterus? What structure is affected in order to cause dyskinetic cerebral palsy?

A
91
Q

What are two notable conditions that patients with cerebral palsy are at higher risk for?

A
92
Q

What are three important elements of supportive care for patients with cerebral palsy? What are elements of prevention in pregnancies that are at risk?

A
93
Q

What is the most common risk factor for the development of glial or meningeal neoplasms?

A

Radiation

94
Q

Patients with HIV/AIDS are at risk for development of what primary CNS tumor?

A

Primary CNS lymphoma

95
Q

What is the most common presentation for a low grade glioma?

A

Seizures

96
Q

What is the most common location for a pilocytic astrocytoma? What notable disease is it associated with? How ar they treated?

A
97
Q

What three criteria are used by the WHO to classify CNS tumors?

A

1) Cell type origin
2) Cell behavior
3) Molecular characteristics

98
Q

What differentiates a low grade tumor from a high grade tumor? Where do pilocytic astrocytoma and glioblastoma rank on the WHO CNS tumor criternia?

A
99
Q

How does a CNS tumor burden spread?

A

Direct infiltration of the surrounding tissue

Note that it does not dissemiante in either blood or lymph

100
Q

What are two major histological findings in glioblastoma?

A
101
Q

What type of tumor is responsible for the butterfly-shaped lesion seen here?

A

Glioblastoma

102
Q

What physical exam finding would be expected in a frontal lobe tumor?

A

Snout reflex pout reflex

103
Q

What WHO grades can be applied to a meningioma? What significant radiological finding is pathognomonic?

A
104
Q

T/F: A meningioma does not typically require surgical resection

A

True

105
Q

T/F: The following findings may indicate an elevated risk for stroke

A

False, they carry an increased risk for seizure

106
Q

What are the three most common sites of primary cancer? Combined, what percentage of brain metastases is comprised of those from these three cancers?

A
107
Q

Proclivity for metastatic tumors to hematogenously translocate to what area of the brain increased seizure risk?

A

Grey-white matter junction

108
Q

What types of hemoglobin would be expected in the following conditions, and what explains differences from normal:
Normal
Sickle cell trait
Sickle cell anemia (SCA)
Hemoglobin SC disease
SCA with hydroxyurea

A
109
Q

How can Parkinson dementia be most easily differentiated from Lewy Body dementia? How does the movement disorder of the latter differ from the former? Which type of dementia is consistant with visual hallucinations and fluctuations of symptoms?

A
110
Q

What abnormality is visible in these images? What diseases can they be found in? What three notable substances make up these abnormalities? In which two CNS locations they be found?

A
111
Q

Why do some Parkinsonian patients receiving pharmacotherapy have symptoms mimicking Lewy body dementia?

A

Parkinson disease is typically treated with L-dopa or dopamine agonists, which can have the side effect of visual hallucinations.

112
Q

Are visual hallucinations common in Alzheimer dementia?

A

No, they occur at a rate of roughly 5-15% of patients.

113
Q

The frequency of what allele increases risk for Alzheimers and Parkinsonian dementia?

A

The apolopoprotein E4 alle

114
Q

What is the preferred atypical antipsychotic medication for a patient with a movement disorder such as Parkinson disease?

A

Quietiapine/Seroquel

115
Q

What is pseudodementia of depression?

A

The mimicking of dementia by depression symptoms, causing patients to feel as if their memory is declining. This is common and treatable.

116
Q

What is multi-infarct dementia?

A
117
Q

What is Frontotemporal Dementia (FTD), previously known as Pick’s disease? What is it often confused with?

A

FTD presents with personality change, altered social behavior and sometimes with progressive aphasia. It tends to be more rapidly progressive than Dementia of Alzheimers type or DAT, with which it is often confused.

FTD presents in the 50-60’s, about 10-15 years earlier on average than DAT.

118
Q

What is the primary component of amyloid plaques? What larger protein is this derived from? What are neurofibrillary tangles?

A
119
Q

What is indicated by the blue and black arrows in this image? (Bielschowsky silver stain)

A

Blue arrows: Neurofibrillary tangles
Black arrows: Threads

120
Q

What is abnormal in this image? (Bielschowsky silver stain)

A

Amyloid plaque

121
Q

What are the three criteria used in the diagnosis of Somatic Symptom Disorder?

A
122
Q

What are the 6 criteria for Illness Anxiety Disorder? (maybe just familiarize)

A

D. Excessive health related-behaviors or maladaptive avoidance
E. Preoccupation for over 6 months (specific illness fear may change over time)
F. Not better explained by another disorder

123
Q

What are the four criteria of Conversion disorder?

A
124
Q

What are the four criteria of Factitious Disorder Imposed on Self?

A
125
Q

How does Factitious Disorder Imposed on Self differ from Factitious Disorder Imposed on Another?

A

FDIA involves the same criteria but on another inidividual, usually a vulnerable child or adult.

126
Q

What is malingering? What disorder can it be a symptom of?

A
127
Q

Using the diagram, explain how the hypothalamus exerts sympathetic activity on the retina:

A

Good job!

128
Q

Which nucleus of the hypothalamus is reesponsible for efferent connections to the cortex regarding wakefulness?

A
129
Q

What different major emotion is processed by the amygdala versus the septal nucleus?

A
130
Q

What is the first major nucleus of the frontal cholingergic systems? What are its 3 major functions?

A
131
Q

Where is the Nucleus Basalis of Meynert located? What process affecting it is related to Alzheimer’s dementia or AD? What are 4 notable signs of injury/atrophy? What is the major class of drugs used to treat injury/atrophy (usually due to AD)?

A
132
Q

What are the 3 anatomical divions of the amygdala?

A
133
Q

Which subdivision(s) of the amygdala use the ventral amygdalofugal fibers? Which use the stria terminalis?

A
134
Q

What are two major functions of the septal nucleus? What happens to its function with aging?

A
135
Q

What are the three main mechanisms of traumatic brain injury or TBI?

A
136
Q

What are the subtypes of *skull fracture” and intracranial lesions (two subtypes each)? What are examples of each subtype?

A
137
Q

What type of skull fracture is seen here?

A

Linear

138
Q

What type of skull fracture is seen here?

A

Depressed

139
Q

What type of skull fracture is seen here?

A

Comminuted

140
Q

What areas may be injured in a basilar skull fracture? What is the classic sign of a BSF?

A

It can be a fracture of the orbital roof, sphenoid bone, or petro-mastroid portion of temporal bone

Battle sign or Racoon eyes

141
Q

What type of skull fracture is seen here?

A

Basilar

142
Q

What are the typical treatments for the following types of skull fractures?
Linear
Comminuted
Depressed
Basilar
Open

A
143
Q

What are the three sections of the Glascow Coma Scale? What scores constitute a mild, moderate, or severe score?

A
144
Q

What is the main timeframe for primary vs secondary injury in a TBI? Which is a more common cause of mortality?

A
145
Q

What is the main difference between a vasogenic edema and cytotoxic edema? Which has a greater effect on white matter tracts? What are two examples of causes of each type of edema?

A
146
Q

What are the three main symptoms of the Cushing reflex? What brings it on? Why shouldn’t blood pressure not be lowered in a patient in this situation (i.e. subdural hemotoma)?

A

It is brought on by very high ICP

Don’t bring down the blood pressure, because it will lead to low cerebral perfusion pressure and lead to secondary injury*.

147
Q

What are three components of early management of patients with TBI?

A
148
Q

What are the three elements of manamgement of severe TBI (after early management)? Above what level should cerebral perfusion pressure be maintained?

A
149
Q

What are first and second tier management for elevated ICP in the context of a TBI?

A
150
Q

What type of arteriosclerosis are represented by the arteries on the middle and right of the photo?

A
151
Q

What type of hemorrhages are seen here? What is the classic cause? What type of athero/arterisclerosis is most common?

A
152
Q

What are the four types of vessel pathologies seen here? Which layers of the vessel wall are affected in each?

A
153
Q

Are cerebral aneurysms more likely to be found in anterior or posterior circulation?

A
154
Q

What are the three characteristics present in 97% of ruptured aneurysms?

A
155
Q

What type of aneurysm can be seen on this CT?

A

Berry aneurysms

156
Q

What is the range of values on the Hunt and Hess scale? What is the meaning of each value?

A
157
Q

What is the major concern during initial stabilization of a subarachnoid hemorrhage? What is the percent change of this event within 14 days? Within 6 months?

A
158
Q

What are 2 treatment options for ruptured aneurysms?

A

Microsurgical clipping
Endovascular coiling

159
Q

What is the major concern post-oepration on an aneurysm? What range of days can it occur during the post-op period? What are peak days for concern?

A
160
Q

What are arterio-venous malformations (AVM)?

A

Congenital malformation of cerebral blood vessels, arising during fetal development.

For example, some lack capillary networks, and move directly from arteries to veins. Essentially acts as a shunt, and denies blood flow to areas of brain.

161
Q

What are three notable treatments for AVM?

A
162
Q

What are the three components of the Spetzler-Martin grade scale (used for evaluating arterio-venous malformations)?

A

1) Size of nidus
2) Eloquence of adjacent brain
3) Venous drainage

163
Q

What effect does carbamazepine have on its own metabolism?

A

It induces its own metabolism, leading to increased clearance and shortened serum half life. Increases in daily doseage are necessary to maintain stable levels.

164
Q

How are allodynia, hyperpathia, and hyperalgesia different?

A

Allodynia: pain from a typically non-painful stimulus

Hyperalgesia: increased pain from a typically painful stimulus

Hyperpathia: increased response to all or multiple sensory stimuli

165
Q

Pupils that react to consent but not to light are pathognomonic for what pathlogy?

A

Syphilis

166
Q

What percentage of strokes of ischemic vs. hemorrhagic? What is the best first test in suspected stroke?

A
167
Q

Patients with what medical disorder are at significant risk for a primary CNS lymphoma?

A

HIV/AIDS

168
Q

What WHO grade of tumor is benign?

A

Only grade 1 is truly benign; grade 2 is low grade but prognosis is much worse

169
Q

How does the the acronym “I WATCH DEATH” help explain etiologies of delirium?

A
170
Q

What are severeal differentiating factors between delirium and dementia?

A
171
Q

What is a significant feature of Mild cognitive impairment that is NOT shared with dementia?

A
172
Q

In a patient with dementia symptoms, the following MRI findings would most likely indicate what etiology of dementia?

A

Vascular dementia

173
Q

What are differentiating pathologies, MRI findings, and common features to each of these types of dementia?
Vascular cognitive impairment
Frontotemporal dementia
Lewy body diesase (DLB & PDD)
NPH
Creutzfeldt Jakob disease

A
174
Q

Briefly describe each of the following dementia clinical syndromes:
Amnestic
Posterior Cortical Atrophy
Dysexecutive
Corticobasal Syndrome
Behavioral Variant
Primary Progressive Aphasia

A
175
Q

What are the 3 types of primary progressive aphasia (a type of dementia clinical syndrome)?

A
176
Q

What molecule deficiency is associated with narcolepsy?

A

Hypocretin-1 (orexin A) in the lateral nucleus of the Hypothalamus

177
Q

What imaging should be done first in suspected subarachnoid hemorrhage? If it returns normal, what should be done?

A
178
Q

What is the normal timeline for stevens johnson syndrome after starting an offending medication? What percentage of the body is affected for it to be considered TEN?

A

1-3 weeks

More than 30%

179
Q

What signs are typically seen with organophosphate poisoning?

A

Muscarinic effects

180
Q

What is the go to treatment for organophosphate poisoning?

A

Atropine and pralidoxime

181
Q
A

B&B (9 decks)

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