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Neuro/MSK/Psych > Cerebrovascular dz and infections > Flashcards

Cerebrovascular dz and infections Flashcards

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1
Q

What conditions would you see with a ACA infarct?

A

UMN weakness and sensory loss

Contralateral hemiplegia
Contra LEG more

Alien hand syndrome = semiautomatic movements of contra arm

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2
Q

What conditions would you see with a PCA infarct?

A

Contralateral homonymous hemianopia

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3
Q

What conditions would you see with a MCA infarct?

A

Aphasia
Hemineglect
Hemianopia

Face-arm/face-arm-leg sensorimotor loss

Gaze preference TOWARD side of lesion

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4
Q

What are the most common cerebrovascular DOs?

A

Global ischemia
Embolism
HTN Intraparenchymal hemorrhage
Ruptured aneurysm

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5
Q

What are the 2 types of reduction in blood flow? Describe them.

A

Global ischemia = generalized reduction of perfusion (cardiac arrest, schock, hypotension, etc.)

Focal ischemia = localized (occlusion, atherosclerosis, etc.)

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6
Q

What does a watershed infarct look like? What happens b/w ACA-MCA and MCA-PCA?

A

Sickle-shaped band of necrosis

ACA-MCA = probs with internal carotid (proximal arm and leg weakness, transcortical aphasia)

MCA-PCA = probs with visual processing

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7
Q

For watershed infarcts, what are the 2 patterns of border zone infarcts?

A

Cortical border zone infarctions = cortex and adjacent white matter at ACA/MCA, MCA/PCA

Internal border zone infarctions = deep white matter of corona radiata b/w lentriculostriate/MCA

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8
Q

What sx would you see with a carotid stenosis?

A

Contralateral Face-arm/ leg weakness

Contra sensory changes

Contra visual field defects

Aphasia or neglect

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9
Q

Where are the sites of primary thrombosis? What is an atheroma?

A

Carotid bifurcation
Origin of MCA
Either end on basilar a.

Atheroma = intimal lesion (lipid core with fibrous cap), rupture –> exposes blood to thrombogenic substances

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10
Q

What are the sources of emboli? Which is most affected by embolic infarction?

A

Air emboli = deep sea divers

Septic emboli = bacterial endocarditis

Fat/cholesterol emboli = trauma to long bones (shower emboli)

Marantic emboli = proteinaceous from NBTE, hypercoaguable states - amniotic fluid emboli

MCA = most affected

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11
Q

How would you describe a TIA? Typical duration? What if it is longer? What is it a warning sign of? What aret he mechanisms?

A

It is a NEURO EMERGENCY described as a deficit of <24 hrs caused by temporary brain ischemia

Typical duration = 10 min
If longer, produces some permanent cell death

Warning sign of potential larger ischemic injury

Mechanisms = Embolus, Thrombus, Vasospasm

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12
Q

What are the 2 types of Strokes? Describe them.

A

Hemorrhagic (RED) = intracerebral, SAH; emboli; secondary to reperfusion of damaged vessels

Ischemic (PALE) = thrombus, inadequate blood supply, can have hemorrhagic conversion

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13
Q

What conditions can arise from hypertensive cerebrovascular dz?

A

Lacunar infarcts

Slit hemorrhages

Hypertensive encephalopathy

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14
Q

Describe lacunar infarcts. What a.?

A

Lenticulostriate a. (caudate and putamen) –> pure motor hemiparesis
Lake-like

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15
Q

Describe HTN encephalopathy. How do you get it? Associations?

A

Caused by Malignant HTN

Assoc with Deep brain parenchymal hemorrhage

Vascular multi-infarct dementia
Binswagner (subcortical white matter myelin and axon loss)

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16
Q

What is Charcot-Bouchard microaneurysm assoc with? Where are they located?

A

Chronic HTN

Basal ganglia

17
Q

What is CAA? Similar to?

A

Cerebral amyloid angiopathy = lobar hemorrhage

Similar to ALZ = deposits a-B-amyloid in walls of vessels = microbleeds

18
Q

What is CADASIL? What occurt? What gene? Characteristics?

A

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

Recurrent strokes and dementia

NOTCH3 gene

Detectable at 35 yo with infarcts 10 yrs later

Thickening of media and adventitia, loss of sm cells, PAS+

19
Q

Mycotic aneurysms can occur with vascular invasion of what fungi?

A

Mucor
Aspergillus
Candida

20
Q

When and in who are aneurysms most like to rupture?

A

Fifth decade

Females

21
Q

Where (artery wise) are AVMs most common in the brain? What happens to the parenchyma underneath?

A

MCA and posterior branches

No functional cortex under AVM

22
Q

What are the 4 principle routes to infection? Which one is most common?

A

Hematogenous (most common, arterial mostly)

Direct implantation (trauma, congenital)

Local extension (sinus, teeth, etc)

Peripheral nervous system (virus - rabies, herpes zoster)

23
Q

How does Tuberculus meningitis spread?

A

Seeding CSF from subepidural or submeningeal granulomas

24
Q

How do Herpes Simplex/Zoster and Rabies spread?

A

Herpes simplex/Zoster = Latent infection of sensory ganglia, replicate in schwann cells, ascend to CNS within SENSORY nerves

Rabies = bind at/near acetylcholine receptors at NMJ and ascend to CNS via MOTOR nerves

25
Q

What is an important factor in the pathogenesis of CNS infections and in selection of ABX therapy?

A

Relative impermeability of brain capillaries to immunoglobins, complement, and ABX

26
Q

What are the various types of meningitis? Describe them.

A

Meningoencephalitis

Chemical meningitis = nonbacterial, subarachnoid space

Acute pyogenic = bacterial

Aseptic = viral

Chronic = tuberculosis, spirochetes or cryptococcus

27
Q

What is the CNS response to infection? What is it accelerated by, slowed by?

A

Cerebral edema

Infection –> loss of capillary integrity with transudation of intravascular fluid into brain

Accelerated by = products released by living and lysed bacteria

Slowed and reversed by corticosteroids

28
Q

What bacterial meningitis is located near the saggital sinus? Basal location?

A

Sag sinus = pneumococcal meningitis

Basal = H. Influenza

29
Q

In acute meningitis, what cell occupy the subarachnoid space? What is focal cerebritis?

A

PMNs

FC = inflamm cells infiltrate wall of veins and extend into brain substance

30
Q

What conditions can occur with acute meningitis?

A

Ventriculitis
Focal cerebritis

Phlebitis –> venous thrombosis and hemorrhagic infarct

Leptomeningeal fibrosis –> hydrocephalous

Pneumococcal meningitis –> chronic adhesive arachnoiditis

31
Q

What are complications of bacterial meningitis?

A

Sz

Encephalitis

Hearing loss, blindness, paralysis

Fulminant especially with meningiococcemia, rash

Adrenal hemorrhage –> death = Waterhouse-Friderichsen syndrome

32
Q

Interpret CSF test results for bacterial vs. viral meningitis.

A

Bacterial = turbid, increased neutrophils (PMNs), Glucose DECREASED, Protein increased

Viral = clear, Lymphocytes/mono increased, glucose NL, Protein NL or decreased slightly

33
Q

What bacterial pathogens are common in acute meningitis for neonates, 3m-2yo unvacc, adolescent, elderly?

A

Neonates = E.coli, Group B strep

3m-2yo unvacc = H. Influenza type B

Adolescent = N. Meningitis

Elderly = Strep pneumo, Listeria

34
Q

How do brain abscesses present? What does the CSF look like? Complications? Tx?

A

Progressive focal neuro deficits, increased ICP

CSF = high WBC, high protein, and normal glucose

Complications = rupture with ventriculitis or meningitis and thrombosis

Tx = surgical drainage and ABX

Neuro/MSK/Psych (3 decks)

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