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Week 5 - Neuro > Neuro Diseases / Disorders > Flashcards

Neuro Diseases / Disorders Flashcards

1
Q

epilepsy

A

disorder with intermittent, unpredictable, repeated, unprovoked seizures

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2
Q

seizure

A

physical manifestation of abnormal electrical activity in the brain - uncontrolled coordinated firing of neurons in certain area of brain with or without change in level of consciousness

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3
Q

convulsion

A

type of seizure with activity in area of brain that controls movement, includes involuntary muscle movement

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4
Q

epilepsy facts

A

1% of US pop, 2/3 starting in childhood especially during first year of life, increases again after 60, most common pediatric neurological disorder

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5
Q

EEG

A

electroencephalogram, ambulatory EEG - cap with electrodes that records activity over time and shows activity disturbances even if a seizure does not take place, Tx based on type of seizure

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6
Q

normal EEG

A

coordinated peaks and valleys

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7
Q

generalized epilepsy EEG

A

constant peaks and valleys

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8
Q

generalized seizures

A

generalized bilateral, symmetrical, no local onset, includes grand mal and petit mal

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9
Q

gran mal seizure

A

type of generalized seizure, bilateraly, symmetrical, no focal onset, tonic, clonic, tonic-clonic

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10
Q

petit mal

A

type of generalized seizure, loss of consciousness only

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11
Q

complex petit mal

A

type of generalized seizure, mostly loss of consciousness with brief tonic / clonic / automatic movements

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12
Q

tonic

A

tensing of muscles

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13
Q

clonic

A

as in clonus, contracting and relaxing muscles

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14
Q

partial / focal seizure

A

local onset, includes simple or complex focal seizures

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15
Q

simple focal seizure

A

no loss of consciousness / altered psychic function, includes motor, autonomic, pure psychic (bizarre behavior)

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16
Q

motor simple focal seizure

A

focal onset, no loss of consciousness / altered psychic function, frontal lobe origin, tonic, clonic, tonic-clonic, benign childhood epilepsy

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17
Q

complex focal seizure

A

focal onset, impaired consciousness, begin as simple partial and progress to impaired consciousness

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18
Q

types of partial / focal seizures

A

simple, complex, partial secondarily generalized

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19
Q

types of generalizes seizures

A

generalized tonic-clonic (grand mal), absence (petit mal), tonic, atonic, clonic and myoclonic, infantile spasm

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20
Q

primary generalized epilepsies

A

age dependent, generalized 2.5-4 Hz bifrontal spikes, polyspikes and slow wave discharge, no structural abnormality, normal intelligence, often genetic component

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21
Q

secondarily generalized seizure

A

start local and evolve into tonic-clonic seizures, no genetic component, result of brain disease due to congenital malformation or metabolic defect

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22
Q

partial / focal seizure

A

no loss of consciousness, classified by clinical manifestation (motor, sensory, autonomic, psychic), aura (subjective preceding manifestation - is the initial phase of focal seizure) - can lead into altered consciousness

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23
Q

convulsive seizures

A

commonly tonic-clonic (grand mal), less commonly pure tonic, pure clonic, clonic-tonic-clonic generalized

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24
Q

nonconvulsive seizures

A

brief lapse / absence in consciousness (petit mal), also can include minor motor (brief myoclonic, atonic, tonic)

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25
Q

status epileticus

A

acute, prolonged epileptic crisis - seizure >30 min or repeated seizures for >30 min without recovery, tonic clonic seizures are most concerning, if airway compromised may have brain damage / death from - hypoxia / cardiac arrhythmia / lactic acidosis

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26
Q

non-convulsive status epileticus

A

neuronal damage due to increased metabolic activity is debated, possible ischemic brain damage in elderly

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27
Q

tonic - clonic seizures

A

type of generalized seizure across entire brian (grand mal), aura often precedes, tonic phase - loss of consciousness and tense muscles, clonic phase - muscles contract and relax rapidly causing convulsions

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28
Q

myoclonic seizures

A

more common in 0-14 yrs, brief involuntary twitching of muscles or group of muscles, can be hiccups, often occur after waking up

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29
Q

partial seizures

A

limited to specific area in brain, can include any movement, sensory or auditory symptom, simple - 30-60sec with no loss of consciousness, complex partial -1-2min with aura and automatisms and lack of awareness

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30
Q

absence seizures

A

more common in 0-14 yrs, petit mal, no aura, abrupt onset, brief, prompt recovery, altered consciousness, no extreme muscle effects, may effect learning

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31
Q

complex partial seizures

A

more common 15-65 yrs, effect larger area of brain than simple partial seizures, can’t interact, no memory of event, altered consciousness

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32
Q

dysprosody

A

can speak, abnormal expression of emotion/tone/inflection/emphasis, inability to interpret and comprehend emotion/tone in speech, caused by lesion to right (nondominant) hem opposite Broca’s area

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33
Q

frontal lobe lesion

A

problems with executive function - like mood, orientation, concentration, appropriate social behavior

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34
Q

Glasgow Coma Scale

A

use if pt unresponsive in ER,

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35
Q

suicide

A

males - more violent and successful, females - less violent and successful

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36
Q

attention deficit hyperactivity disorder

A

developmental, three traits - attention prob / hyperactive / impulsiveness occurring together, starts before 7 yrs, 5-10% school kids, decreases into adulthood, prob kids misdiagnosed, 6 attention or 6 hyperactive symptoms present for 6 mnths in more than one setting and causing difficulties, parent / teacher questionnaire, IQ / psych test / evaluation

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37
Q

attention deficit hyperactivity disorder

A

deficient NE and DA activity in pathways - Tx raising DA / NE reduces symptoms

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38
Q

ADHD NE pathway

A

locus coeruleus -> frontal and limbic cortex, focus, attention, working memory

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39
Q

ADHD DA pathway - mesocortical

A

tegmentum -> frontal and limbic cortex, mediates cognitive functions

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40
Q

ADHD DA pathway - nigrostriatal

A

substantia nigra -> striatum, motor hyperactivity / impulsiveness

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41
Q

ADHD DA pathway - mesolimbic

A

ventral tegmentum -> nucleus accumbens, euphoria (reason for abuse)

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42
Q

alzheimer disease (AD)

A

cortical degeneration, dementia, impaired higher function, altered mood / behavior, progressive, disorientation, memory loss, aphasia, elderly, 40% > 80 yrs, destruction of cholinergic (ACh) neurons in neocortex / amygdala / hippocampus / frontal cortex (from nucleus basalis of Meynert)

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43
Q

alzheimer microscopic

A

neurofibrillary tangles inside neurons, beta amyloid polypeptide plaques

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44
Q

neurofibrillary tangles

A

tau proteins around neuron microtubules, interfere with axonal transport leading to cell death

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45
Q

beta amyloid polypeptid plaques

A

nucleus basalis of meynert neurons over produces, accumulate at synapse, interferes with cholinergic transmission leading to die off of innervated areas

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46
Q

alzheimer progression

A

memory problems - neuronal loss in nucleus basalis of meynert, 3 years - cell damage / loss spreads (diagnosis and loss of independence), 3-6 years - neocortex heavy cell death, 3 years - pt death

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47
Q

metastatic brain tumors

A

70% of CNS tumors, 25% 0f tumors spread to the brain, lung, breast, kidney, liver, and melanoma primary cancers (determines tx)

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48
Q

primary brain tumors

A

30% of brain tumors, adults, giloblastoma multiforme and meningioma

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49
Q

metastasis brain tumors

A

well circumscribed, multiple sites, junction of gray and white matter (meningeal carcinomatosis)

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50
Q

primary brain tumors

A

poorly circumscribed (infiltrating fingers), single, location by type

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51
Q

CNS tumors in children

A

second most common neoplasm in children, medulloblastoma and astrocytoma

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52
Q

typical CNS tumor tx

A

surgery first if possible, followed by adjuvant chemo or radiation following to remove residual cancer cells

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53
Q

brain tumor locations

A

kids - 70% in posterior fossa, adults - 70% supratentorial (hemispheric)

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54
Q

WHO grade 1

A

brain tumor with low proliferative potential, cured with surgery alone

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55
Q

WHO grade 2

A

brain tumor that is infiltrative but low proliferative activity, fingers but slow growing, 5 year survival

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56
Q

WHO grade 3

A

brain tumor that is malignant, showing nuclear atypia and mitotic activity - looks disorganized, 2-3 year survival

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57
Q

WHO grade 4

A

brain tumor that is malignant, mitotically active, necrosis prone in center, rapid pre and post operative progression, elderly GBM not more than 1 year

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58
Q

brain tumor grading

A

graded with localizing / imaging, further graded during surgery, affected by age / location / performance / radiological features / extent of resection / proliferation / genetic alterations (no blood / urine markers)

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59
Q

radiation for brain tumors

A

breaks DNA in tumor cell, many breaks = cell death, some may be resistant to radiation

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60
Q

gliomas / astrocytomas

A

astrocytes / oligodendrocytes / ependymal cells, high grade = fatal, infiltrative

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61
Q

glioblastoma multiforma (GBM)

A

highest grade astrocytoma, most malignant

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62
Q

glioma symtoms

A

headache, seizures, memory loss, changes in behavior

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63
Q

pilocytic astrocytoma

A

grade I astrocytoma, benign, low proliferative, children (0-19), posterior fossa, cerebellum, good prognosis, cystic, long hair-like bipolar cells, rosenthal fibers (corkscrew - eosinophilic - made GFAP proteins), biphasic - loose/inactive and dense/active cell areas, hole = edema

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64
Q

pilocytic astrocytoma genetics

A

targeted therapy to the BRAF (RAF) mutation that prevents the formation of nuclear transcription factors (BRAF also common in melanoma)

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65
Q

diffuse astrocytoma

A

grade II astrocytoma, low proliferative, infiltrative, turns into secondary gliobastoma (bad), slow progress, becomes anaplastic, surgery followed by radiation (for slow cells), 20-39 yrs old

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66
Q

diffuse astrocytoma microscope

A

more cells, mostly astrocytes with round nuclei

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67
Q

fibrillary astrocytoma

A

fibers running through it, many astrocytes with round nuclei

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68
Q

gemistocytic astrocytoma

A

many large astrocytes filled with GFAP protein, astrocytoma variant

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69
Q

genetic mutations and astrocytic gliomas

A

diffuse astroctyoma with P53 mutation worse survival rate, oligodendroglioma with 1p/19q loss mutation better survival

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70
Q

anaplastic astrocytoma

A

grade III, more cellular regions / pleomorphism / mitoses, cells filled with GFAP fibers, cells in undifferentiated state, enlarged nuclei

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71
Q

GFAP

A

glial fibrillary acidic proteins, intermediate filament in mature astroctye, modulates motility and shape, activated after injury causing astrogliosis

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72
Q

glioblastoma

A

grade IV astrocytoma, varied appearance, necrosis, vascular proliferation

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73
Q

primary glioblastoma

A

most common primary brain tumor, adults 45-75 yrs, 10 mnth survival, butterfly glioma crosses midline, pseudopalisading necrosis

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74
Q

glioblastoma mutliforme GBM

A

slow progessing neuro deficit (motor weakness), headache, ICP, headache, nausea, vomting, cognitive impairment, seizures, 45-75 yrs

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75
Q

glioblastoma butterfly lesion

A

travels across corpus callosum

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76
Q

pseudopalisading nuclei

A

look stacked, not in location that normally has stacked nuclei, found in glioblastoma

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77
Q

secondary glioblastoma

A

can arise from diffuse astrocytoma or anaplastic astrocytoma, commonly from precursor cells with IDH1/2 mutation and TP53 mutation

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78
Q

oligodendroglioma

A

less common, adults, seizures, 5-10 yr survival, 1p/19q deletion improves survival, circumscribed, heminspheric, round nuclie with cytoplasmic halos (fried egg), delicate capillaries, calcified

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79
Q

ependymoma

A

line vesciles in CNS, children, fourth ventricle, less common adults in spine, slow growing, 4 yr survival, CSF dissemination, solid or papillary, round nuclei, dense fibrillary, canals, pseudorosettes, rosettes, try to make little ventricles

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80
Q

rosettes

A

canals/lumen surrounded by cells in ependymoma

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81
Q

vascular pseudorosettes

A

vessels surrounded by fibers in ependymoma

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82
Q

Homer-Wright rosette

A

cells surrounding nerupil, in medulloblastoma and primitive neuroectodermal tumor (PNET)

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83
Q

Flexner - Wintersteiner rosette

A

retinoblastoma, cells around cytoplasmic extensions of tumor

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84
Q

medulloblastoma

A

primitive neurons, children, cerebellum, very radiosensitive, i(17q) mutation has poor prognosis, well circumscribed, small, dark , elongated, anaplastic, Homer-Wright rosettes, pseudorosettes, headache, AM vomiting, back pain, motion problems, 0-10 yrs esp males

85
Q

i(17)(q10) mutation

A

very bad prognosis in medulloblastoma, isochrome 17 i(17) part of chromosome breaks off / flips / reattaches at q10

86
Q

primary brain lymphoma

A

rare, immunosuppressed, detectable in CSF, aggressive, responds poorly to chemo, large, B cell lymphoma (EBV), multiple nodules, necrotic foci, periventricular, hard to tell from trophasomes in HIV

87
Q

ring enhancing lesion

A

multiple, cerebral and basal, from toxoplasmosis, immunocrompromised

88
Q

meningioma

A

second most common primary brain tumor, benign, arachnoid cells, slow growing, surgery, attached to dura, compresses brain, syncytial pattern (cells in circular bundles), psammoma bodies (calcium deposits)

89
Q

schwannoma

A

third most common brain tumor, CN VII at cerebellopontine angle, hearing loss, tinnitus, good prognosis, surgery, normal palisading, hypercellular and hypocellular areas

90
Q

retinoblastoma

A

sporadic are unilateral, familial are bilateral and associated with osteosarcoma, Flexner-Wintersteiner rosettes

91
Q

craniopharyngioma

A

odontogenic epithelium, children - young adults, calcified, benign, recurring, compression of optic chiasm - vision problems

92
Q

myxopapillary variant of ependymoma

A

adults, in spinal cord (filum terminale), myxoid mass, mucinous/myxoid degeneration, well circumscribed, surgery

93
Q

depression

A

sadness, pessimism, worry, agitation, withdrawal, somatic concerns, sleep / eat changes, mental slowing - 15% suicide, 4th most common complaint in primary care, 1/10 has it, medical care over utilizers

94
Q

mania

A

high energy, euphoria, rapid speech, racing thoughts, decreased sleep, hypersexual, excessive goal behavior

95
Q

unipolar depression

A

once, recurrent separated by euthymia

96
Q

bipolar disorder

A

mood alternation between depression and mania, may be separated by euthymia, cycle rapidly, occur concurrently

97
Q

amine hypothesis of depression

A

insensitive amine receptors or deficient amine synthesis / storage / release, amines = norepinephrine and serotonin

98
Q

amine hypothesis of mania

A

excess amines (norepinephrine, serotonin)

99
Q

problem with amine hypothesis of mood disorders

A

mismatch between time course, neurochemical effects 1-2 days, clinical improvement 10-21 days

100
Q

psychosis

A

psychiatric illness, DA levels increased, locus in limbic system, tx block DA receptors, tx causes parkinsonism

101
Q

parkinsonism

A

neurologic illness, DA levels decreased, locus in striatum, tx increase DA levels, tx causes psychosis

102
Q

psychosis

A

psychiatric illness, impaired behavior / coherent thought / comprehension of reality, delusions and hallucinations, includes schizo / delirium / dementia / bipolar / psychotic depression / drug induced

103
Q

schizophrenia positive symptoms

A

delusions, hallucinations (auditory), disorganized throught / speech, disorganized behavior, catatonic - gained functions

104
Q

schizophrenia negative symptoms

A

lack of emotion / interest in life / flattening / alogia (inability to speak) / social skills - loss of functions

105
Q

schizophrenia cognitive symptoms

A

disorganized thought, slow thought, difficulty understanding, poor concentration, poor memory, difficulty expressing/integrating thought

106
Q

dopamine hypothesis of schizophrenia

A

caused by increased DA, increased D2 receptor activity causes psychoses - proof: amphetamines increase DA and cause psychosis, first gen anti-psychotics block DA receptors as seen to work, weakness - DA levels only seem to be related to positive schizoprenia symptoms

107
Q

four DA pathways in the brain

A
  1. mesolimbic, 2. mesocortical, 3. nigrostriatal, 4. tuberoinfundibular
108
Q

mesolimbic DA pathway

A

tegmentum -> nucleus accumbens, mediates positive symptoms of schizophrenia, block DA D2 receptors and symptoms decrease, drugs that increase DA (amphetamine / cocaine) cause positive symptoms in this pathway

109
Q

mesocortical DA pathway

A

tegmentum -> frontal and limbic cortex, mediates negative symptoms of schizophrenia, decreased DA levels produces / worsens negative symptoms, why neg symptoms are worsened by antipsychotics that block DA receptors - second gen antipsychotics affect both DA and 5HT receptors and are better at tx for neg symptoms

110
Q

nigrostriatal DA pathway

A

substantia nigra -> basal nuclei, regulates posture and voluntary movement, first generation antipsychotics block DA receptors producing parkinsonism, second gen antipsychotics less likely to produce parkinsonism

111
Q

tuberinfundibular DA pathway

A

hypothalamus -> anterior pituitary, DA inhibits prolactin release, first gen antipsychotic females may experience galactorrhea / amenorrhea / sexual dysfunction

112
Q

at risk of abusing prescription drugs

A

doctors, nurses, dentists, PAs, vets, pharmacists, prof pts

113
Q

abused prescription drugs

A

opiods, anxiolytic-sedative-hypnotics, CNS stimulants

114
Q

abused opioids

A

morphine, codeine, heroin, oxycodone, hydrocodone, tx for pain, temporary bliss with indifference to environment

115
Q

abused anxiolytic-sedative-hypnotics

A

more benzodiazepines (diazepam, alprazolam) than barbiturates, tx for anxiety and insomnia, produces disinhibition euphoria - white collar “alcoholsim”

116
Q

CNS stimulants

A

methylxanthine (caffeine), andrenomimetics (dextroamphetamine, methamphetamine, methylphenidate - ritalin), tx for narcolepsy and ADHD, increases wakefulness / attentiveness / performance - used in college

117
Q

other drugs of abuse

A

cocaine, phencyclidine, LSD, MDMA, ketamine, flunitrazepam, ethanol, nicotine, caffeine

118
Q

psychoactive drugs

A

alter behavior, seek drugs that alter consciousness in pleasurable way, society determines what is drug abuse

119
Q

tolerance

A

decreased effect of drug, increased dose needed

120
Q

cross tolerance

A

tolerance to drugs in same group

121
Q

opioids tolerance

A

rapid - analgesia; slow - miosis, constipation

122
Q

barbiturates / benzodiazepines

A

fast - sleep; slow - antiseizure, lethal

123
Q

psychological dependence

A

feel a sense of doom if can’t get a drug

124
Q

physical dependence

A

withdrawal

125
Q

addiction

A

not same as physical dependence, addiction becomes central to life / behaviors

126
Q

drug misuse

A

drug within medical context, ill advised patterns of prescribing

127
Q

drug abuse

A

use drugs for psychic effects, non-medical, disapproval from society

128
Q

type I drug abuse

A

pt has hx of drug abuse

129
Q

type II drug abuse

A

takes drug for medical reason, becomes addicted, rare if not a myth - esp if meds properly managed

130
Q

prescription drug abuse rates

A

rising, 60% of drug related ER visits, 70% of drug related deaths from prescription drugs, 30% of street drugs

131
Q

sources of street prescription drugs

A

clandestine labs, pharmacy burglary, diversion from health professionals

132
Q

should be aware or Rx drug abuse because…

A

social responsibility (know drug action and uses), professional responsibility (right dose to right pt for right reason), personal responsibility (protect medical practice)

133
Q

MN physician Rx abuse discipline

A

rx to pt with known addiction, unmonitored opioid rx, rx with no physical exam, rx with known drug interaction, rx in known contraindications

134
Q

type of doctor Rx drug abusers target

A

dishonest, disabled, deceived, dated

135
Q

protect Rx pad

A

safe storage, use one at a time, numbered consecutively, do not sign in advance, write in ink, write out amount of meds, no notes/ memos, do not leave unattended

136
Q

drug seeking behaviors

A

ask for specific meds, request more, claim allergy and lack of efficacy, evasive answers, traveling through town, no primary doc, lost prescription, late afternoon apt on Friday

137
Q

Rx drug abuser scams

A

altered script by adding zero, sick grandpa with allergy to certain meds, accomplice in the health care office, pt posed as doctor to pharmacy

138
Q

when in doubt…

A

ask for photo ID, verify DEA number on a script, hang a notice in your office, do not confuse drug seeking with unresolved pain

139
Q

brain injury

A

leading cause of death/disability ages 1-44 yrs

140
Q

primary brain injury

A

happens in first 4 hrs, leads to secondary brain injury which the part you want to prevent

141
Q

coma

A

sustained altered consciousness, pathologic (unless iatrogenic)

142
Q

Glasgow coma scale

A

14

143
Q

Monro-Kellie hypothesis

A

19

144
Q

CT scan

A

CT is like 360 x-ray that measures density in Houndsfield unit (fluid 0HU, air -1000HU, bone 1000HU), normal brain 40-70HU, image of choice for brain injury, head CT takes 8 sec, good at looking for blood to decide if there is a pressure problem

145
Q

normal on CT

A

calcified choroid plexus / pineal gland

146
Q

pressure problem in skull

A

must determine, if present = emergency, CT scan, GCS, too much blood / brain / CSF - only so much blood and CSF can be subtracted, then brain starts to be damaged (must do something before this happens) - brain will herniate into foramen magnum

147
Q

most common subarachnoid hemorage

A

trauma by far, then nontrauma aneurysm - happens in evening - those that survive have clotted off

148
Q

fully absructed hyprocephalus

A

dead in 6 hrs, make 18 ml CSF / hr

149
Q

bad on CT

A

midline shift, whiter hyperdense areas (acute blood) or darker hypodense (chronic blood), gyri and sulci compressed and not showing

150
Q

acute blood on CT

A

hyperdense - looks white

151
Q

chronic blood on CT

A

hypodense - looks dark

152
Q

change the rules for brain swelling

A

take away some bone and leave off, allows brain to swell, done especially with gun shot wounds

153
Q

subdural hemorrhage

A

fuzzy edges, follows curve of the skull

154
Q

epidural hematoma

A

lens shaped mass, edges demarcated, venous bleed (survive), arterial bleed (don’t live)

155
Q

hydrocephalus from blood filled ventricles

A

shunt out of head, only put in with low GCS

156
Q

cerebrovascular disease

A

stroke, three mechanisms thrombosis (clot at location)/embolism (moving object - usually clot)/hemorrhage (can form mass or go into subarachnoid space), lack of blood or ruptured vessel are two main mechanisms, acute focal neurological loss, 3rd cause of death in US

157
Q

global cerebral ischemia

A

hypotension, mild - transient confusion, severe - persistent vegitative state/brain death, can last 4min without damage, watershed infarcts - temporary hypotension causes loss of blood to area where major vessel branches end - thin gray matter, loss of brain mass

158
Q

global cerebral ischemia histology

A

first day - red neurons/neutrophils, then - necrosis/macrophages/vessel proliferation/gliosis, after weeks - loss of necrotic tissue leaving open space

159
Q

areas susceptible to hypoxia

A

watershed areas (where branches of two larger arteries meet), lamina (where areas of cortex meet)

160
Q

watershed infarcts

A

edges of two major arteries, looks like hypodense dark diffuse area on CT

161
Q

focal cerebral ischemia

A

obstructed blood flow to one area of brain, two types - ischemic and hemorrhagic

162
Q

ischemic focal infarct

A

thrombi develops in vessel, from atherosclerotic plaque, look pale, broader circular area affected

163
Q

hemorrhagic infarct

A

look red, from emboli (moves) and reperfusion injury from weakened vessel, emboli often from heart esp with atrial fibrillation / patent foramen ovale, more focal area affected

164
Q

transient ischemic attacks

A

temporary with no signs on imaging, are harbingers of ischemic infarct later

165
Q

thrombosis causes

A

atherosclorsis, carotid bifurcation/middle cerebral artery origin/ends of basilar artery, leads to ischemic infarction

166
Q

embolism causes

A

blood clot, heart/carotid/marrow/fat/tumor, middle cerebral artery branch points, lead to hemorrhagic infarction

167
Q

ischemic infarct gross

A

days - white, swollen, 10 days - gelatinous, outlines visible, weeks - liquefaction and cavitation

168
Q

hemorrhagic infarct gross changes

A

punctate hemorrhages or big hematoma, resolution and cavitation

169
Q

focal infarct micro changes

A

hours - days: red neurons, edema, swelling, neutrophils, macrophages; weeks - gliosis, more macrophages, dense gliosis, new capillaries, ischemic and hemorrhagic infarcts look microscopically the same but hemorrhagic has extravasated blood

170
Q

lacunar infarct

A

causes lacunar infarcts in deep cerebral vessels (basal ganglia, deep white matter, brainstem), tiny infarct with tissue loss/macrophages/gliosis, can be clinically silent or cause severe impairment, caused by arteriolar sclerosis that occludes vessel

171
Q

slit hemorrhage

A

hypertension ruptures little vessels, little hemorrhages, leave brown slit-like cavity, hemosiderin-laden/lipid laden macrophages and gliosis

172
Q

acute hypertensive encephalopathy

A

acute malignant hypertension, diffuse effect - confusion / convulsion / coma, increasing ICP, swollen brain with petechia and fibrinoid necrosis on arterioles

173
Q

hypertensive cerebrovascular disease

A

lacunar infarct, slit hemorrhage, acute hypertensive encephalopathy

174
Q

intracranial hemorrhage

A

anywhere in/around brain, subdural/epidural hemorrhage is usually from trauma, hemorrhage in parenchyma / subarachnoid space usually from cerebrovascular disease

175
Q

parenchymal hemorrhage

A

around 60, high mortality, commonly rupture of small intraparenchymal vessel, ganglioic or cortico lobar, commonly caused by hypertension

176
Q

hypertension as cause of parenchymal hemorrhage

A

HT causes atherosclorsis, hyaline arteriolosclerosis, frank necrosis, weakens vessel walls, sometimes time aneurysms (Charcot-Bouchard microaneurysm)

177
Q

subarachnoid hemorrhage

A

rupture of berry aneurysm common, other causes - rupture of intracranial hemorrhage into subarachnoid space, coagulopathy, vascular malformation, tumors, traumatic hematoma extension

178
Q

berry aneurysm

A

mostly sporadic, risks - smoking and hypertension, grow slowly, >1cm have 50% risk of bleed / year, common at arterial branch points, thin sac, high mortality with rupture

179
Q

subarachnoid hemorrhage clinical findings

A

severe headache (worst ever), loss of consciousness in minutes, death in 25-50%, regain consciousness if survive, risk of vasospastic injury or communicating hydrocephalus do to blockage near CSF resorption location

180
Q

alzheimer disease

A

degenerative disease of cortex neurons, dementia, gross atrophy of brain, microscopic plaques and tangles, 3-20 yr prognosis

181
Q

alzheimer symptoms

A

most common cause of dementia in elderly, 40% at 85 yrs, early - forgetful in higher level functions/mood/behavior, then - disorientation/memory loss/ motor skill loss, 5-10 year - profound disability/mute/immobile, death common from infection (pneumonia)

182
Q

alzheimer progression - parts of the brain

A

affected first - hippocampus (memory) and language (temporal/frontal cortex), later - entire cortex from front to back with disease progression (personality/mood changes, then motor changes)

183
Q

neuritic plaques - alzheimer

A

dilated, tortuous neurites around amyloid core, contain beta amyloid

184
Q

neurofibrillary tangles - alzheimer

A

bundles of filament in neuron cytoplasm, made of tau, MAP2, and ubiquitin

185
Q

other microscopic changes - alzheimer

A

neuronal loss, gliosis, cerebral amyloid angiopathy, granulovasuolar degeneration, Hirano bodies collections of actin

186
Q

alzheimer pathogensis

A

deposition of Abeta peptides from abnormal processing of amyloid precursor protein, Abeta accumulates making amyloid aggregate that are neurotoxic and inflammatory, tau accumulation in tangles seems to be secondary (other dementia diseases have tau deposition on microtubules)

187
Q

normal amyloid precursor protein cleavage

A

usually cleaved into three parts, abnormal secretase enzymes, Abeta portion of cleavage forms aggregate

188
Q

pick disease

A

rare, distinct, progressive dementia, frontal lobe signs (personality change) and temporal lobe signs (language problems), severe atrophy in both lobes, neuronal loss / swelling, pick bodies with tau protein in neuronal cytoplasm - does not progress to occipital lobe

189
Q

parkinson

A

degeneration of substantia nigra neurons, tremor, rigidity, bradykinesia, atrophy of substantia nigra, Lewy bodies in cells, slightly shortened life

190
Q

parkinson symptoms

A

facial mask, stooped posture, slowed voluntary movement, festinating gait, rigidity, pill-rolling tremor, responds to L-DOPA, autonomic/cognitive dysfunction, some dementia, L-DOPA tx symptoms but does not slow disease

191
Q

parkinson morphology

A

palor of substantia nigra, loss of pigmented neurons in substantia nigra, lewy bodies in cells in nucleus of Meynert, neuronal loss

192
Q

parkinson pathogenesis

A

5 associated genes, unknown mechanism, possibly alpha-synuclein (in lewy bodies), degeneration of DA neurons

193
Q

deep brain stimulation with parkison / severe depression

A

electrode in brain, stops inhibition of thalamus allowing motor movement, wear pace maker under the skin

194
Q

amyotrophic lateral sclerosis (ALS - lough gerigs disease)

A

degeneration of motor neurons, rapid progressing weakness/spasticity/dysphagia, sensory and cognitive function intact, death within 2-3 years from resp compromise

195
Q

ALS clinical

A

early - hand weakness, arm/leg spacticity, twitch, slurred speech; then - atrophy, fasciculations, creeping paralysis; later - resp muscles effected and infection

196
Q

progressive muscular atrophy

A

lower motor neurons only

197
Q

progressive bulbar palsy

A

upper motor neurons, symptoms around mouth / face, progress faster

198
Q

ALS pathogenesis

A

superoxide dysmutase mutation in some inherited cases, impaired ubiquitin 2 housekeeping protein in all cases, misfolded / accumulated proteins?

199
Q

ALS morphology

A

thin anterior roots of spinal cord, anterior horn neurons reduced, skeletal muscle atrophy, degeneration of corticospinal tract

200
Q

continuum of cognition

A

normal aging, mild cognitive impairment, dementia

201
Q

alzheimer pathophysiological cascade

A

age/gentics + cerebrovascular risks -> Abeta amyloid accumulation -> synpatic dysfunction / glial activation / tangle formation / neuronal death -> cognitive decline

202
Q

alzheimer course

A

preclinical - amyloid beta accumulation / synpatic dysfunction / tau neuronal injury; mild cognitive decline - tau neuronal injury / brain structures affected / cognition effected; dementia - cognition / clinical function; preclinical almost matches normal aging decline until mild cognitive decline presents

203
Q

biggest risk factor for alzheimer with hallucinations/delusions

A

isolation

204
Q

gioblastoma multiforme microscopic

A

hyperchromatic (mitotic), pleomorphic, psuedopallisading around necrosis, vascular proliferation, anaplastic sheets

205
Q

gliobastoma multiforme tx course

A

resection, radiation, temozolomide chemo if candidate and O-methylguanine methyltransferase gene is methylated

206
Q

glioblastoma multiform

A

psuedopalisading cells around necrotic tissue, anaplastic cells, hyperplastic vessels, 60-70 yrs, 12 mnth survival, grade 4 by definition, grow fast, butterfly lesion

207
Q

glioblastoma multiform symptoms

A

seizures, headache (positional), neuro deficits - weakness, dysphagia, dyspraxia, ataxia, increased ICP, CN problems

208
Q

tumor vs necrotic abscess vs infectious abscess on MRI

A

if infectious - shows in labs results too, abcess likely better demarcated than infiltrative tumor, necrosis darker on T1 MRI - know true difference by biopsy

Week 5 - Neuro (3 decks)

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