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Maddy - NMSP Exam II > Path - Cerebrovascular Disease > Flashcards

Path - Cerebrovascular Disease Flashcards

1
Q

what are the symptomatic effects of an anterior cerebral artery ACA) infarction

A

upper motor neuron-type weakness and cortical-type sensory loss

contralateral leg is affected more than the arm or face

“alien hand” syndrome (semiautomatic movements of the contralateral arm are not under voluntary control)

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2
Q

what are the symptomatic effects of a posterior cerebral artery (PCA) infarct

A

contralateral homonymous hemianopia

loss of half vision in both eyes on the contralateral half

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3
Q

what are the symptomatic effects of a middle cerebral artery (MCA) infarct

A

1) aphasia
2) hemineglect (patients fail to be aware of items to one side of space)
3) hemianopia
4) face-arm or face-arm-leg sensorimotor loss
5) gaze preference is toward the side of the lesion

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4
Q

what are causes of global ischemia

A

cardiac arrest, shock, severe hypotension

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5
Q

what are causes of focal ischemia

A

1) embolic or thrombotic arterial occlusion

2) atherosclerosis in HTN

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6
Q

damage to a watershed area produces what kind of necrosis

A

sickle-shaped band of necrosis

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7
Q

infarction in the ACA-MCA watershed area produces what sx

A

proximal arm and leg weakness

transcortical aphasia (language issues)

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8
Q

infarction in the MCA-PCA watershed area produces what sx

A

higher-order visual processing deficits

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9
Q

how do ACA-MCA watershed area infarcts occur

A

occlusion of the internal carotid a.

hypotension in a pt with carotid stenosis

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10
Q

what is the main cause of stenosis of the internal carotid a.

A

atherosclerosis

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11
Q

sx of carotid stenosis

A

1) contralateral face-arm or farm-arm-leg weakness
2) contralateral sensory changes
3) contralateral visual field defects
4) aphasia or neglect

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12
Q

thrombi formed in the internal carotid a. can embolize where?

A

MCA, ACA, ophthalmic artery

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13
Q

what are the primary sites of thrombosis

A

1) carotid bifurcation
2) origin of MCA
3) either end of basilar a.

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14
Q

describe how atherosclerosis can cause thrombosis

A

atheroma (intimal lesion, lipid core covered by fibrous cap) –> ruptures –> exposes blood to thrombogenic substance –> thrombosis/clot

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15
Q

rupture of an atherosclerotic plaque resulting in thrombosis causes what kind of infarct

A

wedge-shaped

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16
Q

describe paradoxical embolus and what can cause it

A

thromboembolus formed in the venous system travels to the arterial system

  • patent foramen ovale (PFO)
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17
Q

describe causes of:

  • air emboli
  • septic emboli
  • fat or cholesterols emboli
  • merantic emboli
  • amniotic fluid emboli
A
  • air emboli: deep sea divers
  • septic emboli: bacterial endocarditis
  • fat or cholesterols emboli: trauma to long bones
  • merantic emboli: noninfectious endocarditis (NBTE)
  • amniotic fluid emboli: childbirth
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18
Q

list causes of hyper coagulable states that can cause thrombosis

A

1) heritable (protein S and C deficiency, antithrombin III deficiency)
2) dehydration
3) adenocarcioma/malignancies
4) surgery, trauma, childbirth
5) DIC
6) hematologic disorder (sickle cell, leukemia, polycythemia)
7) vasculitis

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19
Q

causes of TIAs

A
  • migraines
  • seizures
  • cardiac arrhythmias
  • hypoglycemia in elderly
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20
Q

what is the duration of TIAs

how do different durations cause different brain deficits

A

less than 24 hours
- typically ~10 mins tho

> 10 mins: some permanent cell death

> 1 hour: usually small infarcts, complete functional recovery can occur within 1 day

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21
Q

what are the potential mechanisms behind a TIA

A

1) an embolus temporarily occludes, then dissolves
2) in situ thrombus formation
3) vasospasm

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22
Q

compare the two types of stroke

A

1) hemorrhagic (red): emboli associated

2) ischemic (pale): thrombus associated

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23
Q

compare thrombus and emboli

A

thrombus: blood clot that forms in a vein
emboli: anything that travels through the blood vessels until it reaches a vessel that is too small to let it pass

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24
Q

what event can occur with an ischemic stroke causing more severe consequences

A

hemorrhagic conversion

- fragile vessels rupture leading to secondary hemorrhage

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25
Q

with what disease do lacunar infarcts occur

A

hypertensive cerebrovascular dz

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26
Q

what are slit hemorrhges

A

small caliber penetrating vessels causing slit-like cavities

  • the slit is surrounded by pigment laden macrophages and gliosis
  • seen in HTN cerebrovascular dz
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27
Q

sx of vascular multi-infarct dementia

A
  • dementia
  • gait abnormlaities
  • pseudo bulbar signs (frequent, involuntary and uncontrollable outbursts of crying or laughing)
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28
Q

what is binswanger disease

A

a large area of arteriosclerosis and thromboembolism affecting the blood vessels that supply the white-matter and deep structures of the brain

–> large area of subcortical white matter w/ myelin and white matter loss

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29
Q

what are charcot-bouchard micro aneurysms

A

minute aneurysms in the basal ganglia

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30
Q

what is seen in cerebral amyloid angiopathy (lobar hemorrhage)?

A

beta amyloid deposition in the walls of vessels (same as Alzheimer’s) –> produces microbleeds

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31
Q

what is CADASIL (cerebral autosomal dominant arteriopathy w/ subcortical infarcts and leukoencephalopathy)

A

recurrent strokes and dementia
- first detectable around 35 y/o

Morphology: thickening of media and adventitia, loss of smooth muscle cells, and basophilic PAS+ deposits

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32
Q

what gene is associated with CADASIL

A

NOTCH 3

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33
Q

thickening of media and adventitia, loss of smooth muscle cells, and basophilic PAS+ deposits indicates _____

A

CADASIL (cerebral autosomal dominant arteriopathy w/ subcortical infarcts and leukoencephalopathy)

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34
Q

what is the most frequent cause of subarachnoid hemorrhage

A

rupture of saccular (berry) aneurysm

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35
Q

in what part of the circulation are saccular, mycotic, traumatic, and dissecting aneurysms most often seen

A

anterior

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36
Q

in what part of the circulation are atherosclerotic aneurysms most often seen

A

basilar a.

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37
Q

compare saccular, giant, fusiform, and mycotic aneurysms

A

saccular: bulges from one side of artery
giant: can involve more than one artery, over 2.5cm wide
fusiform: bulges from all sides of an artery, does not have a neck
mycotic: caused by infected artery

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38
Q

in the first few days after a subarachnoid hemorrhage, what are pts are risk for

A

additional ischemic injury from vasospasm affecting vessels bathed in extravasated blood

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39
Q

two tx for aneurysm

A

1) clipping

2) coiling

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40
Q

how do arteriovenous malformations affect the brain parenchyma

A

there is non-functional cortex under an AVM

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41
Q

most common route in CNS infection

A

hematogenous

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42
Q

how does TB meningitis develop

A

by seeding CSF from the sub-epidural or sub-meningeal granulomas

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43
Q

how do herpes simplex and zoster cause CNS infection

A

they produce latent infection of sensory ganglia –> replicate in Schwann cells –> and ascend to the CNS via SENSORY nerves

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44
Q

how does rabies cause CNS infection

A

bings at or near the acetylcholine receptors at the NMJ –> ascends to the CNS via MOTOR nerves

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45
Q

how does the structure of capillaries affect CNS infections

A

no fenestrations or intracellular clefts

they are relatively impermeable to antibodies, complement, and antibiotics

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46
Q

causes of chronic meningitis

A

1) TB
2) spirochetes (neurosyphilis or neuroborreliosis)
3) cryptococcus

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47
Q

what is the CNS response to infection

A

cerebral edema

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48
Q

how can you slow and reverse CNS edema in response to infection

A

corticosteroids

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49
Q

sx of acute (suppurative) meningitis

A
  • HA
  • meningeal irritation signs (kerning, brudzinski)
  • high fever
  • confusion and coma
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50
Q

compare locations between pneumococcal and H. influenzae in where their exudate occurs in meningitis

A

pneumococcal: often densest near sagittal sinus

h. influenzae: basal location

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51
Q

in acute meningitis, what fills the subarachnoid space

A

polymorphonuclear cells (PMNs)

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52
Q

describe the consequences of acute meningitis:

  • ventriculitis
  • focal cerebritis
  • phlebitis
A
  • ventriculitis: inflammation extending into ventricles
  • focal cerebritis: inflammatory cells infiltrate walls of veins and extend into brain substance
  • phlebitis: inflammation of veins leading to venous thrombosis and hemorrhagic infarction
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53
Q

what is a consequence that an occur with pneumococcal meningitis

A

chronic adhesive arachnoiditis

(thickening and adhesions of the leptomeninges in the brain or spinal cord)

“hand soap in your CSF”

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54
Q

what are the presumptive diagnosis from the following gram stains:

  • gram negative diplococci
  • gram positive diplococci
  • gram negative pleomorphic
  • gram positive cocci
  • gram negative bacilli
A
  • gram negative diplococci: Neiserria meningitidis
  • gram positive diplococci: strep pneumonia
  • gram negative pleomorphic: h. influenza
  • gram positive cocci: s. aureus or s. epidermis, streptococci
  • gram negative bacilli: e. ocli or other gram neg
55
Q

what are the three tubes used to test in an LP

A

1st tube: most likely to be contaminated with skin/bacteria
2nd tube: chemistry
3rd tube: cell count

56
Q

compare the following between an LP of bacterial and viral meningitis:

  • gross appearance
  • neutrophil count
  • lymphs/mono count
  • glucose
  • protein
A

1) gross appearance:
- bacteria: cloudy, viral: clear
2) neutrophil count:
- bacteria: much higher
3) lymphs/mono count:
- viruses: much higher
4) glucose:
- greatly decreased in bacterial, normal in viral
5) protein:
- increased in both, but more increased in bacterial

57
Q

describe the following in an LP of a fungal meningitis:

  • CSF appearance
  • dominant cell type
A

CSF appearance: clear

dominant cell type: early: PMNs, late: lymphocytes

58
Q

list the common bacterial pathogens in acute meningitis for the following age groups:

  • neonate
  • 3m-2 y/o unvaccinated
  • adolescent/young adult
  • elderly
A
  • neonate: E. coli, group B strep
  • 3m-2 y/o unvaccinated: H. influenza type B
  • adolescent/young adult: N. meningitides
  • elderly: strep pneumonia and listeria monocytogenes
59
Q

list the common bacterial pathogens in acute meningitis for the following conditions:

  • immunocompromised
  • basilar skull fracture
  • head trauma: post neurosurgery
  • CSF shunt
A
  • immunocompromised: S. pneumonia, N. meningitidis, L. monocytogenes, P. aeruginosa
  • basilar skull fracture: s. pneumonia, h. influenzae, group A beta hemolytic strep
  • head trauma: post neurosurgery: s. aureus, s. epidermis, aerobic gram-neg bacilli (P. aeruginosa)
  • CSF shunt: s. aureus, s. epidermis, aerobic gram-neg bacilli (P. aeruginosa), P. acnes
60
Q

how does a congenital R –> L shunt increase risk for brain abscess

A

it removes the pulmonary filtration of organisms from the blood

61
Q

most common bacterial causes of brain abscesses

A

strep and staph

62
Q

sx of brain abscess

A

progressive focal neurological deficits with sx of increased ICP

63
Q

what does the CSF show in a pt with brain abscess

A

high WBC, high protein, normal glucose

64
Q

describe a subdural empyema

A

bacterial or fungal infection of the skull bones or sinuses that spreads to the subdural space

65
Q

sx of untreated subdural empyema

A

focal neurological signs, lethargy, coma

66
Q

thickened dura is indicative of ____

A

subdural empyema

67
Q

osteomyelitis is associated with what type of abscess

A

extradural abscess

68
Q

how does neisseria cause meningitis

A

colonization in crowded populations (dorms, Baracks, prisons)

–> colonizes the oropharynx and rhino pharynx of asymptomatic carriers –> spreads to CNS

69
Q

clinical manifestations of N. meningitidis

A

rapidly progressive septicemia w/ fever, hypotension, DIC, petechial and purpuric lesions

  • hemorrhagic skin lesions can progress to gangrene
  • hemorrhagic infarction of adrenal glands
70
Q

adrenal gland infarction due to n. meningitidis is characteristic of what dz process

A

waterhouse-friderichsen syndrome

71
Q

sx of chronic meningitis

A
  • fever
  • headache
  • lethargy
  • confusion
  • N/V
  • neck stiffness
72
Q

describe the CSF in chronic meningitis

A
  • elevated protein
  • lymphocytes
  • low glucose level
73
Q

gelatinous or fibrinous exudate in the subarachnoid space is indicative of ____

A

chronic meningitis from TB

74
Q

obliterative endarteritis can occur with what dz processes

A

chronic meningitis from TB

meningovascular neurosyphilis

75
Q

where does chronic meningitis from TB affect the brain

A

it has a predilection for the base of the brain

obliterates the cisterns and encases the cranial nerves

76
Q

what is a tuberculoma

A

a well-circumscribed intraparenchymal mass of TB in the brain causing central caseous necrosis

seen in chronic TB meningitis

77
Q

what kind of stain is used to diagnose TB

A

acid fast stain

78
Q

sx of chronic meningitis from borrelia burgdorferi

A

rash then 4 weeks later neurological sx

  • cranial nerve palsies
  • peripheral neuropathies
79
Q

what is seen in the CSF in chronic meningitis from borrelia burgdorferi

A

antibodies and polymerase chain reaction

80
Q

compare paretic and meningovascular neurosyphylis

A

maningovascular: chronic meningitis at base of brain –> communicating hydrocephalus, obliterative endarteritis
paretic: progressive mental deficits w/ delusions of grandeur that terminate in severe dementia, has iron deposits

81
Q

cause of tabes dorsalis

A

damage to sensory nerves in the dorsal roots

82
Q

“Lightening pains”, absence of deep reflexes, loss of pain sensation, and joint damage (“Charcot joints”) indicate what dz process

A

tabes dorsalis

83
Q

80% of viral causes of aseptic meningitis are caused by _____

A

enteroviruses

84
Q

latent viral meningitis and encephalitis is indicative of what etiologies

A
  • herpes zoster

- progressive multifocal leukoencephalopathy

85
Q

perivascular lymphocytic cuffs are seen in what dz process

A

viral encephalitis

86
Q

sx encephalitis from west nile virus

A

polio like syndrome w/ paralysis

87
Q

CSF in encephalitis from west nile virus

A

colorless, increased pressure, increased protein, normal glucose

  • initially exciting neutrophilic pleocytosis and then rapidly converts to lymphocytosis
88
Q

describe the appearance of the parenchyma in arthropod-borne viral encephalitis (ex: west nile)

A
  • multiple foci of necrosis in both white and gray matter
  • neuronophagia
  • microglial nodules
89
Q

describe appearance of parenchyma in HSV-1 encephalitis

A

necrotizing and hemorrhagic in the inferior and medial temporal lobes

90
Q

histological hallmark of HSC-1 encephalitis

A

cowry type A intranuclear viral inclusions in the neurons and glia

91
Q

hemorrhagic temporal lobes indicates ____

A

HSV-1 encephalitis

92
Q

what is persistent postherpetic neuralgia syndrome

A

persistent pain and painful sensation following non painful stimuli

  • seen with shingles
93
Q

describe how CMS affects the brain parenchyma in utero

A

periventricular necrosis –> severe brain destruction –> microcephaly and periventricular calcification

94
Q

where does CMV localize

A

in paraventricular subependymal regions

95
Q

describe how acute polio affects the spinal cord, and what sx does it elicit

A

mononuclear cel perivascular cuffs and neuronphagia of the anterior horn motor neurons on the spinal cord

–> flaccid paralysis

96
Q

what is post-polio syndrome

A

occurs 25-35 years after resolution of initial illness

progressive weakness w/ decreased muscle mass and pain

97
Q

how does rabies cause CNS effects

A

infection ascends along peripheral nerves from the wound site

98
Q

sx rabies

A
  • malaise, ha, fever
  • local paresthesias around the wound
  • CNS excitability, violent motor responses
  • flaccid paralysis
  • hydrophobia (foaming at the mouth, aversion to swallowing)
99
Q

local paresthesia around a wound is indicative of what infectious agent

A

rabies

100
Q

negri bodies indicate ___

A

rabies

101
Q

compare morphology of acute and chronic HIV meningitis

A

acute: mild lymphocytic meningitis, perivascular inflammation, some myelin loss
chronic: microglial nodules w/ multinucleated giant cells

102
Q

describe the vessels and white matter of the brain in HIV meningitis

A

vessels: abnormally prominent endothelial cells and perivascular foamy or pigment-laden macrophages

white matter: myelin pallor, axonal swelling, gliosis

103
Q

what is IRIS (immune reconstitution inflammatory syndrome)?

A

occurs with antiviral therapy with HIV meningitis
- paradoxical deterioration after starting therapy

–> inflammatory response –> paradoxical exacerbation of symptoms from opportunistic infections

104
Q

why does HIV associated dementia occur

A

because of inflammatory activation of microglial cells

105
Q

increased incidence of primary CNS lymphoma is associated with ____

A

HIV

106
Q

multinucleated giant cells are seen with what etiologies

A
  • HIV
  • herpes
  • TB
107
Q

what causes PML (progressive multifocal leukoencephalopathy)

A

JC polyomavirus

108
Q

what happens in PML (progressive multifocal leukoencephalopathy)

A

JC polyomavirus infects oligodendroglial cells –> demyelination

109
Q

what patients get PML (progressive multifocal leukoencephalopathy)

A

immunosuppressed (HIV+)

110
Q

describe the morphology of the brain in PML (progressive multifocal leukoencephalopathy)

A
  • ill defined destruction of white matter
  • subcortical area of demyelination w/ lipid laden macrophages
  • decreased number of axons
111
Q

principle pathologic effect of PML (progressive multifocal leukoencephalopathy)

A

demyelination

112
Q

what causes subacute sclerosing pancencephalitis (SSPE)

A

paramyxovirus

113
Q

sx of subacute sclerosing pancencephalitis (SSPE)

A

cognitive decline, spasticity of limbs, seizures

114
Q

what pts get subacute sclerosing pancencephalitis (SSPE)

A

non-immunized children or young adults following early-age infection w/ measles

115
Q

morphology of subacute sclerosing pancencephalitis (SSPE)

A
  • widespread gliosis
  • myelin degneration
  • neurofibrillary tangles (like Alzheimers)
116
Q

what pts are at increased risk of getting a mucor infection

A

DM pts

117
Q

what fungi cause vasculitis

what fungi cause parenchymal infection

A

vasculitis: nucor and aspergillosis
parenchymal: candida and crypto coccus

118
Q

what histological hallmark is seen with cryptococcus infection

A

cryptococcal soap bubbles

119
Q

what is seen in the CSF in cryptococcus meningitis

A

cryptococcal polysaccharide antigen

120
Q

what test must be done on the CSF to diagnose cryptococcus

A

india ink preparation

121
Q

what pts get toxoplasmosis gondii

A

HIV, immunosuppressed

pregnant pts

122
Q

what happens to the brain parenchyma in toxoplasmosis infection

A

brain abscess near gray-white junction of cerebral cortex and deep-grey nuclei

123
Q

histological hallmarks in toxoplasmosis infection

A
  • central focus of necrosis
  • petechial hemorrhages
  • vascular proliferation
124
Q

what is seen at the periphery of necrotic zones in toxoplasmosis gondii infection

A

free tachyzoites and encysted bradyzoites

125
Q

what is naegleria fowleri

A

brain eating amoeba

- found in warm freshwater

126
Q

acanthamoeba causes what

A

chronic granulomatous meningoencephalitis

127
Q

what infectious agent causes cerebral malaria

A

plasmodium falciparum

128
Q

sx of Creutzfeldt-jakob dz

A
  • gerstmann-straussler-scheinker syndrome
  • fatal familial insomnia
  • kuru
129
Q

what agent causes Creutzfeldt-jakob dz

A

prior protein (PrP)

130
Q

morphology of Creutzfeldt-jakob dz

A

spongiform change: intracellular vacuoles in neurons and glia

131
Q

what are causes of iatrogenic transmission of Creutzfeldt-jakob dz

A
  • corneal transplant
  • brain implant
  • human growth hormone
132
Q

describe fatal familial insomnia

A

seen in Creutzfeldt-jakob dz

  • initially just sleep disturbances
  • then ataxia, autonomic disturbances, stupor, then coma
  • less than 3 year survival
133
Q

what mutation is associated with fatal familial insomnia

A

aspartate substitution at codon 129

Maddy - NMSP Exam II (12 decks)

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