Pathology II PCC > Chapter 22 > Flashcards

Chapter 22 Flashcards

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1
Q

what happens to the soma when there is reversible neuronal damage? irreversible?

A

reversible: somal swelling
irreversible: somal shrinkage

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2
Q

what happens to the Nissl body when there is reversible neuronal damage? irreversible?

A

reversible: Nissl body displacement
irreversible: loss of Nissl body

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3
Q

red neuron

A

dead neuron
shrunken soma, cerebral edema, loss of nucleolus & Nissl body
occurs bc of acute-hypoxic/ischemic injury

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4
Q

what happens when Astrocytes are injured

A

hypertrophy & hyperplasia

enlarged nucleus, eosinophilic

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5
Q

what happens when oligodendrocytes are injured

A

white matter damage = nuclear swelling
happens in acquired demyelinating disorders & leukodystrophies
enlarged nucleus

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6
Q

what happens when microglia are injured

A

proliferate & enlarge

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7
Q

what happens when ependymal cells are injured

A

ependymal granulations–> infections (CMV)

may involve chorioid plexus bc ependymal cells line ventricles & spinal cord

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8
Q

when do intracellular inclusions occur?

A 
viral infections (rabies = Negri body, CMV = owl's eyes)
parkinson disease = Lewy body
Alzheimers disease = neurofibrillary tangles & beta-amyloid plaques; tau proteins
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9
Q

cerebral edema (general types)

A

vasogenic- BBB disruption, extracellular edema

cytotoxic- glial membrane injury, intracellular edema

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10
Q

hydrocephalus

A

• MC because of disturbed flow/resorption
• 2 years = ↑ ICP, ventricular enlargement
• Hydrocephalus ex vacuo : compensatory: infarct, neurodegeneration
• congenital
• 50% idiopathic
ventriculoatrial shunt
Untreated: lethal tonsillar herniation, respiratory arrest

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11
Q

Brain herniation (general)

A

• ↑ ICP
• Initially: vessel compression & CSF displacement
• Later: cerebrum shifts (herniation)
o ↓ blood supply = infarction; injury = swelling  Dangerous positive feedback loop!

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12
Q

Brain herniation types

A
  1. subfalcine/cingulate (MC)– abnormal posturing, coma
  2. transtentorial/uncinated-CN III (blown pupil); hemiparesis & brainstem compression  Duret hemorrhage (flame-shaped hemorrhage)
  3. Tonsillar–cardiorespiratory arrest
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13
Q

Arnold-Chiari malformations

A

herniation of cerebellar tonsils
Type I (MC)–adults
Type II–infants, more severe, misshapen midline cerebellum

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14
Q

cerebrovascular disease

A

3rd leading cause of mortality in US
MC cause of neurologic morbidity
Stroke = infarction
TIA = No infarction, temporary

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15
Q

ischemia cell response

A

neutrophils (12-48 hrs) –>nuclear fragmentation (48 hrs-2 weeks) –>Macrophages & gliosis (months to years, cavitation)

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16
Q

respirator brain

A

autolysis of neurons caused by mechanical ventilation

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17
Q

Focal cerebral ischemia

A

arterial occlusion = localized ischemia
sustained = infarction
collateral flow limit injury = circle of willis (deep tissues have limited collateral flow)
Emboli (MC): cardiac mural thrombi

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18
Q

MC cause of vessel wall injury

A

HTN

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19
Q

primary brain parenchymal hemorrhage

A

spontaneous

HTN (MC)

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20
Q

“worst HA i’ve ever had”

A

subarachnoid hemorrhage
ruptured saccular/berry aneurysm
MC in anterior circulation & branch points

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21
Q

Arteriovenous malformation

A
  • Tangle of arteries & veins
  • MC cerebrovascular malformations
  • Males
  • Age 10-30
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22
Q

Hypertensive cerebrovascular disease

A
  1. Massive parenchymal hemorrhage
  2. Lacunar infarct: single artery occlusion; silent  devastating
  3. Slit hemorrhage: ruptured small cerebral vessel, ‘slit-like cavity’ remains
  4. Acute hypertensive encephalopathy: global cerebral dysfxn; HA, confusion, vomiting, convulsions, coma
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23
Q

polyarteritis nodosa

A
  • Systemic autoimmune vasculitis
  • Fibrinoid necrosis
  • Small cerebral arteries & heart
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24
Q

1⁰ angiitis of the CNS

A
  • Chronic inflammation
  • Multiple parenchymal & subarachnoid vessels
  • Only Brain & Spinal cord
  • Idiopathic, Males
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25
general CNS trauma
MALES • Silent=frontal • disabling=cord • fatal=brainstem • Damage to parenchyma &/or cerebral vessels • Assess: ABCD (airway, breathing, circulation, disability)
26
Contusion
* Rapid displacement * Impact site = coup injury * Opposite impact site = contrecoup injury * Gyri susceptible, frontal & temporal lobes
27
Laceration
• Tearing of cerebral parenchyma
28
Diffuse axonal injury (DAI)
SERIOUS angular acceleration, shaking • may NOT involve physical impact • causes diffuse WHITE matter/axonal damage • MC near lateral ventricles & brain stem severe edema • Cause of 50% post-traumatic comas
29
concussion
reversible absence of contusion secondary to trauma • Standard neuroimaging studies are NORMAL!! =CT CANNOT confirm presence of concussion!
30
what does a concussion look like on a CT?
IT LOOKS LIKE NOTHING
31
**bonus: What does osteoporosis look like on x-ray?
IT LOOKS LIKE NOTHING; unless 30-40% already gone
32
Epidural hematoma
ARTERY lucid during bleed emergency MC middle meningeal artery
33
subdural hematoma
VEINS shaken baby infants & geriatrics MC self limited
34
MC CNS malformation
Neural tube defects
35
spina bifida occulta
Neural tube defect bony defect asymptomatic
36
myelomeningocele
Neural tube defect extension of CNS thru lumbosacral vertebral defect urinary incontinence
37
anencephaly
Neural tube defect | absence of brain
38
encephalocele
Neural tube defect | CNS diverticulum thru cranium
39
hydromyelia
spinal cord abnormality cavity connected to 4th ventricle
40
syringomyelia
spinal cord abnormality syrinx cyst w/in cord adults
41
1. Intraparenchymal hemorrhage
prematurity, near ventricles, may cause hydrocephalus
42
Infarct (perinatal brain injury)
supratentorial white matter, chalky plaques, possible cyst
43
cerebral palsy
perinatal brain injury NON-progressive motor neuron defect
44
how are infections of NS acquired MC?
hematogenous
45
epidural abscess
'makes the cavity' | cord compression = emergency
46
subdural empyema
'fills an already made cavity with pus' | infxn of skull/sinus = subdural space = emergency
47
meningitis types (list)
acute pyogenic aseptic chronic: insidious onset
48
acute meningitis
HA, nuchal rigidity, photophobia CSF: ↑pressure, ↑neutrophils, ↑proteins (exudate), ↓ glucose, bacterial culture fatal if untreated
49
aseptic meningitis
• nuchal rigidity, pyrexia, ↓ consciousness, cerebral edema --> self-limiting, CSF: ↑ lymphocytes
50
Chronic: insidious onset meningitis
tuberculous: CSF = moderate ↑ WBC’s & ↑ proteins Spirochetal: 3⁰ syphilis or Lyme disease
51
Parenchymal infections
1. bacterial abscess: localized, liquefactive necrosis 2. viral encephalitis: diffuse, assoc w meningitis, poliovirus, varicella-zoster virus 3. fungal: mixed granulomas, meningitis, MC among immunosuppressed
52
Multiple Sclerosis
* MC disorder of myelin * Episodic, ‘relapsing-remitting’, incomplete recovery * White matter lesions (plaques) * Risks: young adults, females, family history
53
Thiamine disorders
* Wernicke-Korsakoff syndrome | * Beriberi: LE paralysis, paresthesia, nystagmus, pain
54
Cobalamin disorder
demyelination
55
hypoglycemia
mimics global hypoxia; hippocampus
56
hyperglycemia
uncrontrolled DM
57
patterns of neuronal loss (dementia)
o Cortex = memory, language, insight/planning o Cerebellum = ataxia o Motor neurons = weakness
58
alzheimer disease
``` • MC cause of dementia in elderly • Brain: β-amyloid plaques o Neurotoxic, Tau proteins insidious/progressive lethal infection: pneumonia • 10% genetic  down syndrome, early onset ```
59
Parkinson Disease
* Parkinsonism tremor, * Damage to dopaminergic neurons  altered CNS synaptic transmission, Substantia nigra, * Lewy bodies--> neuronal inclusions: α-synuclein * Avg onset: 45-65 years * Progressive * Tx: L-DOPA; does not slow progression just treats symptoms, becomes less effective
60
Huntington Disease
* Autosomal dominant * Severe cerebral atrophy  caudate & putamen nuclei, severity depends on degree of neuronal loss; intranuclear inclusions = Huntingtin protein * 1⁰ feature: chorea, entire body ↓ cognition: memory loss = severe dementia * Delayed age of onset: 30-40 years * MC lethal w/in 15 years
61
Amyotrophic Lateral Sclerosis (ALS)
BOTH UMN & LMN death!! • Preserves sensation & **extraocular motor fxn • MC males • Insidious: asymmetric distal extremity weakness • RAPID progression fasciculations: involuntary muscle contraction • Eventual respiratory paralysis: Death  respiratory infxn (pneumonia) • 10% familial;
62
CNS tumors general info
* Spinal more common than cranial * Most are 1⁰  no premalignant stages, non-resectable = bad * Rarely mets outside CNS
63
types of gliomas
astrocytoma (diffuse & pilocytic), oligodendroglioma, ependymoma
64
diffuse astrocytoma
``` Malignant • 80% of adult gliomas • Cerebral • Poorly circumscribed o Glioblastoma = worst BAD prognosis ```
65
pilocytic astrocytoma
benign • Cerebellar, spinal cord • Well circumscribed kids/young adults
66
Oligodendroglioma
benign or malignant cerebral: frontal & temporal adults
67
Ependymoma
• Periventricular region: kids • Spinal canal: adults o NF2
68
medulloblastoma
``` malignant, KIDS MC embryonal malignancy 20% pediatric brain tumors • Only CEREBELLAR • Tx: excision • Similar to PNETS, just in CNS ```
69
primary CNS lymphoma
• Aggressive, extranodal lymphoma • MC CNS tumor in immunosuppressed pts • Spread via ventricles Any age But risk ↑ with age (>60)
70
meningioma
``` • MC benign tumor of adults (FEMALES) • Invasive • Transformed arachnoid cells • Risks: history of irradiation, NF2 • Easily excised Female Adults ```
71
CNS metastasis
* 25% of intracranial tumors * Mets from: lung, breast, melanoma, * Syncytial (whorled) cell clusters
Pathology II PCC
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