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Pathology II PCC > Chapter 22 > Flashcards

Chapter 22 Flashcards

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
Q

general CNS trauma

A

MALES
• Silent=frontal
• disabling=cord
• fatal=brainstem
• Damage to parenchyma &/or cerebral vessels
• Assess: ABCD (airway, breathing, circulation, disability)

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26
Q

Contusion

A
  • Rapid displacement
  • Impact site = coup injury
  • Opposite impact site = contrecoup injury
  • Gyri susceptible, frontal & temporal lobes
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27
Q

Laceration

A

• Tearing of cerebral parenchyma

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28
Q

Diffuse axonal injury (DAI)

A

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

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29
Q

concussion

A

reversible
absence of contusion
secondary to trauma
• Standard neuroimaging studies are NORMAL!! =CT CANNOT confirm presence of concussion!

30
Q

what does a concussion look like on a CT?

A

IT LOOKS LIKE NOTHING

31
Q

**bonus: What does osteoporosis look like on x-ray?

A

IT LOOKS LIKE NOTHING; unless 30-40% already gone

32
Q

Epidural hematoma

A

ARTERY
lucid during bleed
emergency
MC middle meningeal artery

33
Q

subdural hematoma

A

VEINS
shaken baby
infants & geriatrics
MC self limited

34
Q

MC CNS malformation

A

Neural tube defects

35
Q

spina bifida occulta

A

Neural tube defect
bony defect
asymptomatic

36
Q

myelomeningocele

A

Neural tube defect
extension of CNS thru lumbosacral vertebral defect
urinary incontinence

37
Q

anencephaly

A

Neural tube defect

absence of brain

38
Q

encephalocele

A

Neural tube defect

CNS diverticulum thru cranium

39
Q

hydromyelia

A

spinal cord abnormality
cavity
connected to 4th ventricle

40
Q

syringomyelia

A

spinal cord abnormality
syrinx
cyst w/in cord
adults

41
Q
  1. Intraparenchymal hemorrhage
A

prematurity,
near ventricles,
may cause hydrocephalus

42
Q

Infarct (perinatal brain injury)

A

supratentorial white matter,
chalky plaques,
possible cyst

43
Q

cerebral palsy

A

perinatal brain injury
NON-progressive
motor neuron defect

44
Q

how are infections of NS acquired MC?

A

hematogenous

45
Q

epidural abscess

A

‘makes the cavity’

cord compression = emergency

46
Q

subdural empyema

A

‘fills an already made cavity with pus’

infxn of skull/sinus = subdural space = emergency

47
Q

meningitis types (list)

A

acute pyogenic
aseptic
chronic: insidious onset

48
Q

acute meningitis

A

HA, nuchal rigidity, photophobia
CSF: ↑pressure, ↑neutrophils, ↑proteins (exudate), ↓ glucose, bacterial culture
fatal if untreated

49
Q

aseptic meningitis

A

• nuchal rigidity, pyrexia, ↓ consciousness, cerebral edema –> self-limiting,
CSF: ↑ lymphocytes

50
Q

Chronic: insidious onset meningitis

A

tuberculous: CSF = moderate ↑ WBC’s & ↑ proteins
Spirochetal: 3⁰ syphilis or Lyme disease

51
Q

Parenchymal infections

A
  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
Q

Multiple Sclerosis

A
  • MC disorder of myelin
  • Episodic, ‘relapsing-remitting’, incomplete recovery
  • White matter lesions (plaques)
  • Risks: young adults, females, family history
53
Q

Thiamine disorders

A
  • Wernicke-Korsakoff syndrome

* Beriberi: LE paralysis, paresthesia, nystagmus, pain

54
Q

Cobalamin disorder

A

demyelination

55
Q

hypoglycemia

A

mimics global hypoxia; hippocampus

56
Q

hyperglycemia

A

uncrontrolled DM

57
Q

patterns of neuronal loss (dementia)

A

o Cortex = memory, language, insight/planning
o Cerebellum = ataxia
o Motor neurons = weakness

58
Q

alzheimer disease

A 
•	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
Q

Parkinson Disease

A
  • 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
Q

Huntington Disease

A
  • 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
Q

Amyotrophic Lateral Sclerosis (ALS)

A

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
Q

CNS tumors general info

A
  • Spinal more common than cranial
  • Most are 1⁰  no premalignant stages, non-resectable = bad
  • Rarely mets outside CNS
63
Q

types of gliomas

A

astrocytoma (diffuse & pilocytic), oligodendroglioma, ependymoma

64
Q

diffuse astrocytoma

A 
Malignant
•	80% of adult gliomas
•	Cerebral
•	Poorly circumscribed
o	Glioblastoma = worst
BAD prognosis
65
Q

pilocytic astrocytoma

A

benign
• Cerebellar, spinal cord
• Well circumscribed
kids/young adults

66
Q

Oligodendroglioma

A

benign or malignant
cerebral: frontal & temporal
adults

67
Q

Ependymoma

A

• Periventricular region: kids
• Spinal canal: adults
o NF2

68
Q

medulloblastoma

A 
malignant, KIDS
MC embryonal malignancy
20% pediatric brain tumors
•	Only CEREBELLAR
•	Tx: excision
•	Similar to PNETS, just in CNS
69
Q

primary CNS lymphoma

A

• Aggressive, extranodal lymphoma
• MC CNS tumor in immunosuppressed pts
• Spread via ventricles
Any age But risk ↑ with age (>60)

70
Q

meningioma

A 
•	MC benign tumor of adults (FEMALES) 
•	Invasive
•	Transformed arachnoid cells
•	Risks: history of irradiation, NF2
•	Easily excised 
Female
Adults
71
Q

CNS metastasis

A
  • 25% of intracranial tumors
  • Mets from: lung, breast, melanoma,
  • Syncytial (whorled) cell clusters

Pathology II PCC (7 decks)

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